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        <title>Biochemical and Biophysical Research communications via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Biochemical and Biophysical Research communications' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Biochemical+and+Biophysical+Research+communications&t=Biochemical+and+Biophysical+Research+communications&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 13:38:26 +0100</lastBuildDate>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +133 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5619409&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222012%252F01%252F10%252006.18%2522%255BMHDA%255D%253A%25222012%252F01%252F23%252002.12%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222012%252F01%252F10%252006.18%2522%255BEDAT%255D%29%29</link>
            <description>133 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2012/01/23PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5619409</comments>
            <pubDate>Mon, 23 Jan 2012 07:12:00 +0100</pubDate>
            <guid isPermaLink="false">5619409</guid>        </item>
        <item>
            <title>Nuclear localization of lymphocyte-specific protein tyrosine kinase (Lck) and its role in regulating Lim domain only 2 (Lmo2) gene.</title>
            <link>http://www.medworm.com/index.php?rid=5577239&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222369%26dopt%3DAbstract</link>
            <description>Authors: Venkitachalam S, Chueh FY, Yu CL
    Abstract
    Lim domain only protein 2 (Lmo2) is a transcription factor that plays a critical role in the development of T-acute lymphoblastic leukemia (T-ALL). A previous report established a link between Lmo2 expression and the nuclear presence of oncogenic Janus kinase 2 (JAK2), a non-receptor protein tyrosine kinase. The oncogenic JAK2 kinase phosphorylates histone H3 on Tyr 41 that leads to the relief of Lmo2 promoter repression and subsequent gene expression. Similar to JAK2, constitutive activation of lymphocyte-specific protein tyrosine kinase (Lck) has been implicated in lymphoid malignancies. However, it is not known whether oncogenic Lck regulates Lmo2 expression through a similar mechanism. We show here that Lmo2 expression is signi...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577239</comments>
            <pubDate>Tue, 27 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577239</guid>        </item>
        <item>
            <title>Carnosic acid, a pro-electrophilic compound, inhibits LPS-induced activation of microglia.</title>
            <link>http://www.medworm.com/index.php?rid=5577242&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214931%26dopt%3DAbstract</link>
            <description>Authors: Yanagitai M, Itoh S, Kitagawa T, Takenouchi T, Kitani H, Satoh T
    Abstract
    In the previous studies, we reported that carnosic acid (CA) protects cortical neurons by activating the Keap1/Nrf2 pathway, which activation is initiated by S-alkylation of the critical cysteine thiol of the Keap1 protein by the &quot;electrophilic&quot;quinone-type CA. Here, we found that the pro-electrophilic CA inhibited the in vitro lipopolysaccharide (LPS)-induced activation of cells of the mouse microglial cell line MG6. LPS induced the expression of IL-1β and IL-6, typical inflammatory cytokines released from microglial cells. CA inhibited the NO production associated with a decrease in the level of inducible NO synthase. Neither CA nor LPS affected cell survival at the concentrations used here. These...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577242</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577242</guid>        </item>
        <item>
            <title>Traces of certain drug molecules can enhance heme-enzyme catalytic outcomes.</title>
            <link>http://www.medworm.com/index.php?rid=5577241&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214932%26dopt%3DAbstract</link>
            <description>We report that trace amounts (nano- to picomolar concentrations) of dapsone and amiodarone in reaction mixtures of structurally and functionally distinct heme enzymes gave increased product formation rates from diverse substrates. These enhancements are found to be lowered by mild radical quenchers; a lowering well differentiated from heme active site inhibitions. Based on the non-specific nature of the activations in the diverse heme enzyme reactions studied, a generic mechanism is proposed to explain additive-based activity enhancements in heme enzymology.
    PMID: 22214932 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577241</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577241</guid>        </item>
        <item>
            <title>Uridine adenosine tetraphosphate (Up(4)A) is a strong inductor of smooth muscle cell migration via activation of the P2Y(2) receptor and cross-communication to the PDGF receptor.</title>
            <link>http://www.medworm.com/index.php?rid=5577240&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22214933%26dopt%3DAbstract</link>
            <description>In this study, we present substantiate data that Up(4)A exhibits migration stimulating potential probably involving the signaling cascade of MEK1 and ERK1/2 as well as the matrix protein OPN. We further suggest that the initiation of the migration process occurs predominant through direct activation of the P2Y(2) by Up(4)A and via transactivation of the PDGFR.
    PMID: 22214933 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577240</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577240</guid>        </item>
        <item>
            <title>Statins inhibit expression of Thioredoxin reductase 1 in rat and human liver and reduce tumour development.</title>
            <link>http://www.medworm.com/index.php?rid=5577238&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222370%26dopt%3DAbstract</link>
            <description>CONCLUSION: Statin treatment decreases the hepatic expression of TrxR1 in humans and rats. Suppression of TrxR1 expression could explain possible anti-carcinogenic effects of statins. In addition, decreased levels of TrxR1 during statin treatment may shed light on the mechanism of other side-effects of statins.
    PMID: 22222370 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577238</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577238</guid>        </item>
        <item>
            <title>Regulation of enzyme activity of alcohol dehydrogenase through its interactions with pyruvate-ferredoxin oxidoreductase in Thermoanaerobacter tengcongensis.</title>
            <link>http://www.medworm.com/index.php?rid=5577237&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222371%26dopt%3DAbstract</link>
            <description>Authors: Wang Q, Wang Q, Tong W, Bai X, Chen Z, Zhao J, Zhang J, Liu S
    Abstract
    Alcohol dehydrogenases (ADHs) from thermophilic microorganisms are interesting enzymes that have their potential applications in biotechnology and potentially provide insight into the mechanisms of action of thermo-tolerant proteins. The molecular mechanisms of ADHs under thermal stress in vivo have yet to be explored. Herein, we employed a proteomic strategy to survey the possible interactions of secondary-ADH (2-ADH) with other proteins in Thermoanaerobacter tengcongensis (T. tengcongensis) cultured at 75°C and found that 2-ADH, pyruvate-ferredoxin oxidoreductase (PFOR) and several glycolytic enzymes coexisted in a protein complex. Using anion exchange chromatography, the elution profile indicated th...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577237</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577237</guid>        </item>
        <item>
            <title>A natural squamosamide derivative FLZ inhibits homocysteine-induced rat brain microvascular endothelial cells dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5577236&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222372%26dopt%3DAbstract</link>
            <description>Authors: Kang RX, Zhang JJ
    Abstract
    Hyperhomocysteinemia is believed to induce endothelial dysfunction, which is an independent risk factor for atherosclerosis and vascular diseases. Compound FLZ is a novel synthetic squamosamide cyclic analog with several phenolic hydroxy groups, and exhibits strong anti-oxidative and neuroprotective activities in Alzheimer's and Parkinson's models. In the present study, we examined the actions of FLZ against homocysteine-induced injury to primary cultured rat brain microvascular endothelial cell (rBMECs). Cell survival was measured by MTT assay. Cell nuclei were observed by Hoechst 33342 staining. Senescent cells were detected by senescence-associated β-galactosidase (SA-β-gal) staining. Reactive oxygen species (ROS) were measured by 2',7'-dich...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577236</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577236</guid>        </item>
        <item>
            <title>Reduction of nuclear encoded enzymes of mitochondrial energy metabolism in cells devoid of mitochondrial DNA.</title>
            <link>http://www.medworm.com/index.php?rid=5577235&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222373%26dopt%3DAbstract</link>
            <description>Authors: Mueller EE, Mayr JA, Zimmermann FA, Feichtinger RG, Stanger O, Sperl W, Kofler B
    Abstract
    Mitochondrial DNA (mtDNA) depletion syndromes are generally associated with reduced activities of oxidative phosphorylation (OXPHOS) enzymes that contain subunits encoded by mtDNA. Conversely, entirely nuclear encoded mitochondrial enzymes in these syndromes, such as the tricarboxylic acid cycle enzyme citrate synthase (CS) and OXPHOS complex II, usually exhibit normal or compensatory enhanced activities. Here we report that a human cell line devoid of mtDNA (HEK293 ρ(0) cells) has diminished activities of both complex II and CS. This finding indicates the existence of a feedback mechanism in ρ(0) cells that downregulates the expression of entirely nuclear encoded components of mito...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577235</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577235</guid>        </item>
        <item>
            <title>PrP(C) displays an essential protective role from oxidative stress in an astrocyte cell line derived from PrP(C) knockout mice.</title>
            <link>http://www.medworm.com/index.php?rid=5577234&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222374%26dopt%3DAbstract</link>
            <description>In this study, we elucidated the free radical scavenger activity of purified murine PrP(C) in solution and its participation as a cell protector in astrocytes that were subjected to treatment with an oxidant. In vitro and using an EPR spin-trapping technique, we observed that PrP(C) decreased the oxidation of the DMPO trap in a Fenton reaction system (Cu(2+)/ascorbate/H(2)O(2)), which was demonstrated by approximately 70% less DMPO/OH(). In cultured PrP(C)-knockout astrocytes from mice, the absence of PrP(C) caused an increase in intracellular ROS (reactive oxygen species) generation during the first 3h of H(2)O(2) treatment. This rapid increase in ROS disrupted the cell cycle in the PrP(C)-knockout astrocytes, which increased the population of cells in the sub-G1 phase of the cell cycle c...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577234</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577234</guid>        </item>
        <item>
            <title>RAS oncogenic signal upregulates EZH2 in pancreatic cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5577233&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222375%26dopt%3DAbstract</link>
            <description>This study was aimed to define the oncogenic role of EZH2, a histone modifier protein that is induced by oncogenic mutant RAS, using pancreatic cancers of transgenic rats exogenously expressing human mutant RAS. Immunohistochemical observation of preneoplastic or cancerous lesions in the animal model suggested that upregulation of Ezh2 protein is an initiating event in pancreatic carcinogenesis. MEK-inhibition or Elk-1-knockdown downregulated EZH2, and MEK-inhibition or EZH2-knockdown restored expression of a tumor suppressor, RUNX3 in human and rat pancreatic cancer cells activated by the oncogenic RAS. Furthermore, Elk-1- or EZH2-knockdown inhibited growth of the cancer cells. These results strongly suggested that the oncogenic RAS upregulates EZH2 through MEK-ERK signaling, resulted in ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577233</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577233</guid>        </item>
        <item>
            <title>Anti-inflammatory effects of Tat-Annexin protein on ovalbumin-induced airway inflammation in a mouse model of asthma.</title>
            <link>http://www.medworm.com/index.php?rid=5577232&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222376%26dopt%3DAbstract</link>
            <description>Authors: Lee SH, Kim DW, Kim HR, Woo SJ, Kim SM, Jo HS, Jeon SG, Cho SW, Park JH, Won MH, Park J, Eum WS, Choi SY
    Abstract
    Chronic airway inflammation is a key feature of bronchial asthma. Annexin-1 (ANX1) is an anti-inflammatory protein that is an important modulator and plays a key role in inflammation. Although the precise action of ANX1 remains unclear, it has emerged as a potential drug target for inflammatory diseases such as asthma. To examine the protective effects of ANX1 protein on ovalbumin (OVA)-induced asthma in animal models, we used a cell-permeable Tat-ANX1 protein. Mice sensitized and challenged with OVA antigen had an increased amount of cytokines and eosinophils in their bronchoalveolar lavage (BAL) fluid. However, administration of Tat-ANX1 protein before OVA ch...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577232</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577232</guid>        </item>
        <item>
            <title>Identification of the phosphorylation sites on intact TRPM7 channels from mammalian cells.</title>
            <link>http://www.medworm.com/index.php?rid=5577231&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22222377%26dopt%3DAbstract</link>
            <description>Authors: Kim TY, Shin SK, Song MY, Lee JE, Park KS
    Abstract
    Transient receptor potential melastatin 7 (TRPM7) channels are divalent cation-selective ion channels that are permeable to Ca(2+) and Mg(2+). TRPM7 is ubiquitously expressed in vertebrate cells and contains both an ion channel and a kinase domain. TRPM7 plays an important role in regulating cellular homeostatic levels of Ca(2+) and Mg(2+) in mammalian cells. Although studies have shown that the kinase domain of TRPM7 is required for channel activation and can phosphorylate other target proteins, a systematic analysis of intact TRPM7 channel phosphorylation sites expressed in mammalian cells is lacking. We applied mass spectrometric proteomic techniques to identify and characterize the key phosphorylation sites in TRPM7 ch...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5577231</comments>
            <pubDate>Mon, 26 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5577231</guid>        </item>
        <item>
            <title>Endothelin system in intestinal villi: A possible role of endothelin-2/vasoactive intestinal contractor in the maintenance of intestinal architecture.</title>
            <link>http://www.medworm.com/index.php?rid=5558849&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22209790%26dopt%3DAbstract</link>
            <description>Authors: Bianchi M, Adur J, Takizawa S, Saida K, Casco VH
    Abstract
    The endothelin system consists of three ligands (ET-1, ET-2 and ET-3) and at least two receptors (ETA and ETB). In mice ET-2 counterpart is a peptide originally called &quot;vasoactive intestinal contractor&quot; (VIC) for this reason, this peptide is frequently named ET-2/VIC. In intestinal villi, fibroblasts-like cells express endothelin's receptors and response to ET-1 and ET-3 peptides, changing their cellular shape. Several functions have been attributed to these peptides in the &quot;architecture&quot; maintenance of intestinal villi acting over sub-epithelial fibroblasts. Despite this, ET-2/VIC has not been analyzed in depth. In this work we show the intestine gene expression and immunolocalization of ET-1, ET-2 and the ETA and ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5558849</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5558849</guid>        </item>
        <item>
            <title>Differential expression of microRNA and predicted targets in pulmonary sarcoidosis.</title>
            <link>http://www.medworm.com/index.php?rid=5558848&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22209793%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: This study is the first to profile miRNAs in sarcoidosis tissues and to consider their possible roles in disease pathogenesis. Our results suggest that miRNA regulate TGFβ and related WNT pathways in sarcoidosis tissues, pathways previously incriminated in the pathogenesis of sarcoidosis.
    PMID: 22209793 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5558848</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5558848</guid>        </item>
        <item>
            <title>A proteomic study of Hutchinson-Gilford progeria syndrome: Application of 2D-chromotography in a premature aging disease.</title>
            <link>http://www.medworm.com/index.php?rid=5558844&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22210539%26dopt%3DAbstract</link>
            <description>Authors: Wang L, Yang W, Ju W, Wang P, Zhao X, Jenkins EC, Brown WT, Zhong N
    Abstract
    The Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disease characterized by segmental premature aging. Applying a two-dimensional chromatographic proteomic approach, the 2D Protein Fractionation System (PF2D), we identified 30 differentially expressed proteins in cultured HGPS fibroblasts. We categorized them into five groups: methylation, calcium ion binding, cytoskeleton, duplication, and regulation of apoptosis. Among these 30 proteins, 23 were down-regulated, while seven were up-regulated in HGPS fibroblasts as compared to normal fibroblasts. Three differentially expressed cytoskeleton proteins, vimentin, actin, and tubulin, were validated via Western blotting and characterized ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5558844</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5558844</guid>        </item>
        <item>
            <title>Genome-wide identification of cold-responsive and new microRNAs in Populus tomentosa by high-throughput sequencing.</title>
            <link>http://www.medworm.com/index.php?rid=5558847&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22209794%26dopt%3DAbstract</link>
            <description>Authors: Chen L, Zhang Y, Ren Y, Xu J, Zhang Z, Wang Y
    Abstract
    MicroRNAs (miRNAs) are small, non-coding RNAs that regulate the expression of target mRNAs in plant growth, development, abiotic stress responses, and pathogen responses. Cold stress is one of the most common abiotic factors affecting plants, and it adversely affects plant growth, development, and spatial distribution. To understand the roles of miRNAs under cold stress in Populus tomentosa, we constructed two small RNA libraries from plantlets treated or not with cold conditions (4°C for 8h). High-throughput sequencing of the two libraries identified 144 conserved miRNAs belonging to 33 miRNA families and 29 new miRNAs (as well as their corresponding miRNA(∗)s) belonging to 23 miRNA families. Differential expressio...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5558847</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5558847</guid>        </item>
        <item>
            <title>Bone morphogenetic protein (BMP)-4 and BMP-7 suppress granulosa cell apoptosis via different pathways: BMP-4 via PI3K/PDK-1/Akt and BMP-7 via PI3K/PDK-1/PKC.</title>
            <link>http://www.medworm.com/index.php?rid=5558846&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22209843%26dopt%3DAbstract</link>
            <description>Authors: Shimizu T, Kayamori T, Murayama C, Miyamoto A
    Abstract
    BMP-4 and BMP-7 are associated with the suppression of granulosa cell apoptosis. LY294002 (PI3K inhibitor) or UCN-01 (PDK-1 inhibitor) increased the percentage of apoptotic cells in the granulosa cells treated with BMP-4 or BMP-7. The inhibitors of ERK and p38 (SB203580) did not increase the percentage of apoptotic cells in the granulosa cells treated with BMP-4 or BMP-7. Akt inhibitor did not induce apoptosis in the BMP-4-treated granulosa cells, whereas it did induce apoptosis of the BMP-7-treated granulosa cells. In the granulosa cells treated with BMP-4, the PKC inhibitor increased the percentage of apoptotic cells. Our data show that BMP-4 and BMP-7 are associated with granulosa cell survival via several non-Smad ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5558846</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5558846</guid>        </item>
        <item>
            <title>Diospyrin derivative, an anticancer quinonoid, regulates apoptosis at endoplasmic reticulum as well as mitochondria by modulating cytosolic calcium in human breast carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5558845&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22209849%26dopt%3DAbstract</link>
            <description>Authors: Kumar B, Kumar A, Ghosh S, Pandey BN, Mishra KP, Hazra B
    Abstract
    Diospyrin diethylether (D7), a bisnaphthoquinonoid derivative, exhibited an oxidative stress-dependent apoptosis in several human cancer cells and tumor models. The present study was aimed at evaluation of the increase in cytosolic calcium [Ca(2+)](c) leading to the apoptotic cell death triggered by D7 in MCF7 human breast carcinoma cells. A phosphotidylcholine-specific phospholipase C (PC-PLC) inhibitor, viz. U73122, and an antioxidant, viz. N-acetylcysteine, could significantly prevent the D7-induced rise in [Ca(2+)](c) and PC-PLC activity. Using an endoplasmic reticulum (ER)-Ca(2+) mobilizer (thapsigargin) and an ER-IP3R antagonist (heparin), results revealed ER as a major source of [Ca(2+)](c) which led ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5558845</comments>
            <pubDate>Fri, 23 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5558845</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +386 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5528329&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F12%252F05%252004.06%2522%255BMHDA%255D%253A%25222011%252F12%252F22%252016.06%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F12%252F05%252004.06%2522%255BEDAT%255D%29%29</link>
            <description>386 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/12/22PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5528329</comments>
            <pubDate>Thu, 22 Dec 2011 21:06:01 +0100</pubDate>
            <guid isPermaLink="false">5528329</guid>        </item>
        <item>
            <title>Epitope mapping of antibodies against TDP-43 and detection of protease-resistant fragments of pathological TDP-43 in amyotrophic lateral sclerosis and frontotemporal lobar degeneration.</title>
            <link>http://www.medworm.com/index.php?rid=5473539&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22133678%26dopt%3DAbstract</link>
            <description>Authors: Tsuji H, Nonaka T, Yamashita M, Suzukake M, Kametani F, Akiyama H, Mann DM, Tamaoka A, Hasegawa M
    Abstract
    TAR DNA-binding protein of 43kDa (TDP-43) is the major component of the intracellular inclusions in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Here, we show that both monoclonal (60019-2-Ig) and polyclonal (10782-2-AP) anti-TDP-43 antibodies recognize amino acids 203-209 of human TDP-43. The monoclonal antibody labeled human TDP-43 by recognizing Glu204, Asp205 and Arg208, but failed to react with mouse TDP-43. The antibodies stained the abnormally phosphorylated C-terminal fragments of 23-24kDa in addition to normal TDP-43 in ALS and FTLD brains. Immunoblot analysis after protease treatment demonstrated that the epitope of the a...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473539</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473539</guid>        </item>
        <item>
            <title>Negative-feedback regulation of ATP release: ATP release from cardiomyocytes is strictly regulated during ischemia.</title>
            <link>http://www.medworm.com/index.php?rid=5473538&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22133679%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether and how the release of ATP was strictly regulated during ischemia in cultured neonatal rat cardiomyocytes. Ischemia was mimicked by oxygen-glucose deprivation (OGD). Exposure of cardiomyocytes to OGD resulted in an increase in the concentration of extracellular ATP shortly after the onset of OGD (15min), and the increase was reversed by treatment with blockers of maxi-anion channels. Unexpectedly, at 1 and 2h after the onset of OGD, the blocking of maxi-anion channels increased the concentration of extracellular ATP, and the increase was significantly suppressed by co-treatment with blockers of hemichannels, suggesting that ATP release via maxi-anion channels was involved in the suppression of ATP release via hemichannels during persistent OGD. Here w...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473538</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473538</guid>        </item>
        <item>
            <title>The microtubule-associated protein EB1 maintains cell polarity through activation of protein kinase C.</title>
            <link>http://www.medworm.com/index.php?rid=5473552&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120625%26dopt%3DAbstract</link>
            <description>The objective of the current study was to further understand intracellular signaling involved in EB1-dependent cell polarity and motility. B16F10 mouse melanoma cells were depleted of EB1 protein using short hair-pin RNA interference. Correlative live cell-immunofluorescence microscopy was performed to determine localization of WAVE2 and IQGAP1 to protruding versus retracting edges. EB1 knock down caused poor subcellular separation of WAVE2 and IQGAP1, and overall decreased localization. Activation of PKC corrected defects in WAVE2 and IQGAP1 localization, cell spreading and cell shape to levels observed in control cells, but did not correct defects in cell migration. Consistent with these findings, decreased PKC phosphorylation was observed in EB1 knock down cells. These findings support ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473552</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473552</guid>        </item>
        <item>
            <title>Smooth muscle myosin light chain kinase efficiently phosphorylates serine 15 of cardiac myosin regulatory light chain.</title>
            <link>http://www.medworm.com/index.php?rid=5473551&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120626%26dopt%3DAbstract</link>
            <description>Authors: Josephson MP, Sikkink LA, Penheiter AR, Burghardt TP, Ajtai K
    Abstract
    Specific phosphorylation of the human ventricular cardiac myosin regulatory light chain (MYL2) modifies the protein at S15. This modification affects MYL2 secondary structure and modulates the Ca(2+) sensitivity of contraction in cardiac tissue. Smooth muscle myosin light chain kinase (smMLCK) is a ubiquitous kinase prevalent in uterus and present in other contracting tissues including cardiac muscle. The recombinant 130kDa (short) smMLCK phosphorylated S15 in MYL2 in vitro. Specific modification of S15 was verified using the direct detection of the phospho group on S15 with mass spectrometry. SmMLCK also specifically phosphorylated myosin regulatory light chain S15 in porcine ventricular myosin and chi...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473551</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473551</guid>        </item>
        <item>
            <title>The X protein of hepatitis B virus activates hepatoma cell proliferation through repressing melanoma inhibitory activity 2 gene.</title>
            <link>http://www.medworm.com/index.php?rid=5473550&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120627%26dopt%3DAbstract</link>
            <description>In this study, we found that the expression of the newly identified gene melanoma inhibitory activity 2 (MIA2) was reduced by HBV infection invitro and invivo, and that HBV X protein (HBx) plays a major role in this regulation. Recent studies have revealed that MIA2 is a potential tumor suppressor, and that, in most HCCs, MIA2 expression is down-regulated or lost. We found that the knock-down of MIA2 in HepG2 cells activated cell growth and proliferation, suggesting that MIA2 inhibits HCC cell growth and proliferation. In addition, the over-expression of HBx alone induced cell proliferation, whereas MIA2 over-expression impaired the HBx-mediated induction of proliferation. Taken together, our results suggest that HBx activates hepatoma cell growth and proliferation through repression of th...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473550</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473550</guid>        </item>
        <item>
            <title>p53-Independent up-regulation of a TRAIL receptor DR5 by proteasome inhibitors: A mechanism for proteasome inhibitor-enhanced TRAIL-induced apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5473549&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120628%26dopt%3DAbstract</link>
            <description>Authors: Seol DW
    Abstract
    Gliomas are the most common brain tumors in adults and account for more than half of all brain tumors. Despite intensive clinical investigations, average survival for the patients harboring the malignancy has not been significantly improved. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), shown to have potent and cancer-selective killing activity, has drawn considerable attention as a promising anti-cancer therapy. In an attempt to develop TRAIL as an anti-cancer therapy for gliomas, tumor suppressor activity of TRAIL was assessed using human glioma cell lines such as U373MG, U343MG, U87MG and LN18. U343MG, U87MG and LN18 cells were susceptible to TRAIL; however, U373MG cells were completely refractory to TRAIL. Resistance to the applied t...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473549</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473549</guid>        </item>
        <item>
            <title>Detection and mapping of anti-oxidant marker 'Glutathione' in different human brain regions using non-invasive magnetic resonance spectroscopy.</title>
            <link>http://www.medworm.com/index.php?rid=5473548&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120629%26dopt%3DAbstract</link>
            <description>We report in vivo detection of GSH non-invasively from various brain regions (frontal cortex, parietal cortex, hippocampus and cerebellum) in bilateral hemispheres of healthy male and female subjects and from bi-lateral frontal cortex in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD). All AD patients who participated in this study were on medication with cholinesterase inhibitors. Healthy young male (age 26.4±3.0) and healthy young female (age 23.6±2.1) subjects have higher amount of GSH in the parietal cortical region and a specific GSH distribution pattern (parietal cortex&amp;gt;frontal cortex&amp;gt;hippocampus∼cerebellum) has been found. Overall mean GSH content is higher in healthy young female compared to healthy young male subjects and GSH is distributed dif...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473548</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473548</guid>        </item>
        <item>
            <title>Synthetic cyclohexenyl chalcone natural products possess cytotoxic activities against prostate cancer cells and inhibit cysteine cathepsins in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5473547&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120630%26dopt%3DAbstract</link>
            <description>Authors: Majumdar I, Devanabanda A, Fox B, Schwartzman J, Cong H, Porco JA, Christian Weber H
    Abstract
    A number of cyclohexenyl chalcone Diels-Alder natural products possess promising biological properties including strong cytotoxicity in various human cancer cells. Herein, we show that natural products in this class including panduratin A and nicolaioidesin C inhibit cysteine cathepsins as indicated by protease profiling assays and cell-free cathepsin L enzyme assays. Owing to the critical roles of cathepsins in the biology of human tumor progression, invasion, and metastasis, these findings should pave the way for development of novel antitumor agents for use in clinical settings.
    PMID: 22120630 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473547</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473547</guid>        </item>
        <item>
            <title>Overexpression of the human ubiquitin E3 ligase CUL4A alleviates hypoxia-reoxygenation injury in pheochromocytoma (PC12) cells.</title>
            <link>http://www.medworm.com/index.php?rid=5473546&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120631%26dopt%3DAbstract</link>
            <description>In this study, human CUL4A (hCUL4A) was expressed in rat pheochromocytoma (PC12) cells using adenoviral vector-mediated gene transfer, and the effects of hCUL4A expression on hypoxia-reoxygenation injury were investigated. In PC12 cells subjected to hypoxia and reoxygenation, we found that hCUL4A suppresses apoptosis and DNA damage by regulating apoptosis-related proteins and cell cycle regulators (Bcl-2, caspase-3, p53 and p27); consequently, hCUL4A promotes cell survival. Taken together, our results reveal the beneficial effects of hCUL4A in PC12 cells upon hypoxia-reoxygenation injury.
    PMID: 22120631 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473546</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473546</guid>        </item>
        <item>
            <title>Prolonged effect of fluid flow stress on the proliferative activity of mesothelial cells after abrupt discontinuation of fluid streaming.</title>
            <link>http://www.medworm.com/index.php?rid=5473545&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120632%26dopt%3DAbstract</link>
            <description>Authors: Aoki S, Ikeda S, Takezawa T, Kishi T, Makino J, Uchihashi K, Matsunobu A, Noguchi M, Sugihara H, Toda S
    Abstract
    Encapsulating peritoneal sclerosis (EPS) often develops after transfer to hemodialysis and transplantation. Both termination of peritoneal dialysis (PD) and transplantation-related factors are risks implicated in post-PD development of EPS, but the precise mechanism of this late-onset peritoneal fibrosis remains to be elucidated. We previously demonstrated that fluid flow stress induced mesothelial proliferation and epithelial-mesenchymal transition via mitogen-activated protein kinase (MAPK) signaling. Therefore, we speculated that the prolonged bioactive effect of fluid flow stress may affect mesothelial cell kinetics after cessation of fluid streaming. To inv...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473545</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473545</guid>        </item>
        <item>
            <title>Sensitivity of Saccharomyces cerevisiae to the cell-penetrating antifungal peptide PAF26 correlates with endogenous nitric oxide (NO) production.</title>
            <link>http://www.medworm.com/index.php?rid=5473544&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120633%26dopt%3DAbstract</link>
            <description>Authors: Carmona L, Gandía M, López-García B, Marcos JF
    Abstract
    PAF26 is a synthetic fungicidal hexapeptide with cell-penetration properties and non-lytic mode of action. We demonstrate herein the endogenous accumulation of reactive oxygen species (ROS) and nitric oxide (NO) in the model fungus Saccharomyces cerevisiae treated with PAF26. However, the S. cerevisiae deletion mutant of YAP1 - the major inductor of defense to oxidative stress - did not show high sensitivity to PAF26 but rather increased resistance, and its ROS accumulation did not differ from that of the parental strain. Cross-protection experiments suggest that the oxidant H(2)O(2) and PAF26 kill yeast through different pathways. Overall, the data indicate that ROS are not the primary antifungal mechanism of the ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473544</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473544</guid>        </item>
        <item>
            <title>p120-Catenin modulates airway epithelial cell migration induced by cigarette smoke.</title>
            <link>http://www.medworm.com/index.php?rid=5473543&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120634%26dopt%3DAbstract</link>
            <description>Authors: Zhang L, Gallup M, Zlock L, Finkbeiner W, McNamara NA
    Abstract
    Cigarette smoking has been linked to almost all major types of cancer. Emerging evidence suggests that smoking initiates transformed cell growth and migration by disrupting cell-cell interactions in the polarized mucosal epithelium. Together with other adherens junction proteins, p120-catenin (p120ctn) maintains cell-cell adhesion through its direct interaction with E-cadherin. Mislocalization and/or loss of p120ctn have been reported in all lung cancer subtypes and are related to poor prognosis. Here, we showed that p120ctn modulates smoke-induced cell migration via the EGFR/Src-P pathway. Chemical blockade of EGFR/Src signaling inhibited smoke-induced activation of cofilin (an actin severing protein) and prom...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473543</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473543</guid>        </item>
        <item>
            <title>XLGα(olf) regulates expression of p27(Kip1) in a CSN5 and CDK2 dependent manner.</title>
            <link>http://www.medworm.com/index.php?rid=5473542&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120635%26dopt%3DAbstract</link>
            <description>In this study, performance of yeast two-hybrid screening with XLGα(olf) allowed isolation of COP9 signalosome subunit 5 (CSN5), known to regulate the p27(Kip1) protein level through a proteasome dependent pathway. Co-immunoprecipitation experiments followed by Western blotting also showed association of CSN5 with XLGα(olf) linked to down-regulation of p27(Kip1). Gene silencing of endogenous CSN5 by siRNA attenuated the XLGα(olf)-mediated down-regulation, which was also demonstrated to require CDK2. Both knock down of CDK2 and the treatment with a CDK2 inhibitor reversed the reduction of p27(Kip1) due to XLGα(olf). Our findings provide important clues to understanding its physiological functions of XLGα(olf).
    PMID: 22120635 [PubMed - as supplied by publisher] (Source: Biochemical a...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473542</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473542</guid>        </item>
        <item>
            <title>Histone demethylase JMJD2B is required for tumor cell proliferation and survival and is overexpressed in gastric cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5473541&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22133676%26dopt%3DAbstract</link>
            <description>Authors: Li W, Zhao L, Zang W, Liu Z, Chen L, Liu T, Xu D, Jia J
    Abstract
    Epigenetic alterations such as aberrant expression of histone-modifying enzymes have been implicated in tumorigenesis. Jumonji domain containing 2B (JMJD2B) is a newly identified histone demethylase that regulates chromatin structure or gene expression by removing methyl residues from trimethylated lysine 9 on histone H3. Recent observations have shown oncogenic activity of JMJD2B. We explored the functional role of JMJD2B in cancer cell proliferation, survival and tumorigenesis, and determined its expression profile in gastric cancer. Knocking down JMJD2B expression by small interfering RNA (siRNA) in gastric and other cancer cells inhibited cell proliferation and/or induced apoptosis and elevated the expres...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473541</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473541</guid>        </item>
        <item>
            <title>The human Ino80 binds to microtubule via the E-hook of tubulin: Implications for the role in spindle assembly.</title>
            <link>http://www.medworm.com/index.php?rid=5473540&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22133677%26dopt%3DAbstract</link>
            <description>Authors: Park EJ, Hur SK, Lee HS, Lee SA, Kwon J
    Abstract
    The human INO80 chromatin remodeling complex, comprising the Ino80 ATPase (hIno80) and the associated proteins such as Tip49a, has been implicated in a variety of nuclear processes other than transcription. We previously have found that hIno80 interacts with tubulin and co-localizes with the mitotic spindle and is required for spindle formation. To better understand the role of hIno80 in spindle formation, we further investigated the interaction between hIno80 and microtubule. Here, we show that the N-terminal domain, dispensable for the nucleosome remodeling activity, is important for hIno80 to interact with tubulin and co-localize with the spindle. The hIno80 N-terminal domain binds to monomeric tubulin and polymerized mic...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473540</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473540</guid>        </item>
        <item>
            <title>Expression of programmed cell death protein 4 (PDCD4) and miR-21 in urothelial carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5473537&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22133680%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: These data support a decisive role for PDCD4 down regulation in transitional cell carcinoma and confirm miR-21 as a negative regulator for PDCD4. Additionally, PDCD4 immunohistochemical staining turns out to be a possible diagnostic marker for transitional cell carcinoma.
    PMID: 22133680 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473537</comments>
            <pubDate>Sat, 19 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473537</guid>        </item>
        <item>
            <title>Endoplasmic reticulum stress enhances γ-secretase activity.</title>
            <link>http://www.medworm.com/index.php?rid=5473557&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22115781%26dopt%3DAbstract</link>
            <description>In this study, we demonstrate that ER stress induces presenilin-1 expression through activating transcription factor 4 (ATF4), resulting in increased amyloid-β (Aβ) secretion by γ-secretase activity, which is suppressed by quercetin by modifying UPR signaling. This result suggests that ER stress may be stimulated in obesity and type 2 diabetes, thereby enhancing γ-secretase activity that is the underlying molecular mechanism affecting the pathogenesis of AD.
    PMID: 22115781 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473557</comments>
            <pubDate>Wed, 16 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473557</guid>        </item>
        <item>
            <title>Bile salt export pump inhibitors are associated with bile acid-dependent drug-induced toxicity in sandwich-cultured hepatocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5473565&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108051%26dopt%3DAbstract</link>
            <description>This study aimed to construct a model of DILI by employing sandwich-cultured hepatocytes (SCHs). SCHs can be used to assess functions of canalicular transporters such as BSEP and the activity of metabolic enzymes. Here, the impact of 26 test compounds (ritonavir, troglitazone, etc.) was investigated on BA-dependent cytotoxicity in SCHs. SCHs were exposed to each compound for 24h with or without BAs (glycochenodeoxycholic acid, deoxycholic acid, etc.). As a result, BA-dependent toxicity was observed for 11 test compounds in SCHs treated in the presence of BAs, while no signs of toxicity were observed for SCHs treated in the absence of BAs. Of the 11 compounds, nine were known BSEP inhibitors. Moreover, for some compounds, an increase in the severity of BA-dependent toxicity was observed in ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473565</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473565</guid>        </item>
        <item>
            <title>Nicotine induces fibrogenic changes in human liver via nicotinic acetylcholine receptors expressed on hepatic stellate cells.</title>
            <link>http://www.medworm.com/index.php?rid=5473564&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108052%26dopt%3DAbstract</link>
            <description>CONCLUSION: Nicotine at levels in smokers' blood is pro-fibrogenic, through actions on hHSCs expressed nAChRs. Therefore, CS, via its nicotine content, may worsen liver fibrosis. Moreover, nicotinic receptor antagonists may have utility as novel anti-fibrotic agents.
    PMID: 22108052 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473564</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473564</guid>        </item>
        <item>
            <title>Inverse correlation between metallothioneins and hypoxia-inducible factor 1 alpha in colonocytes and experimental colitis.</title>
            <link>http://www.medworm.com/index.php?rid=5473563&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108053%26dopt%3DAbstract</link>
            <description>In this study, we investigated the interaction between HIF-1α and MTs in colonic epithelial cells and during experimental colitis. Dimethyloxalylglycine (DMOG) was used to subject colonocytes to hydroxylase inhibition and HIF-1α stabilization in three experimental models (in vitro, in vivo and ex vivo). Small interfering RNA targeting HIF-1α (siRNA-HIF) and MT (siRNA-MT) together with zinc-mediated MT induction were used to study the interaction between HIF-1α and MT in HT29 cells. Acute colitis was induced in C57BL/6 mice using dextran sulphate sodium. MT expression and HIF-1α protein levels were measured using quantitative real-time PCR and ELISA, respectively. Vascular endothelial growth factor (VEGF) expression was quantified as an indirect measure of HIF-1 transcriptional activit...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473563</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473563</guid>        </item>
        <item>
            <title>The lectin ArtinM binds to mast cells inducing cell activation and mediator release.</title>
            <link>http://www.medworm.com/index.php?rid=5473562&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108054%26dopt%3DAbstract</link>
            <description>This study sought to further investigate the effects of the lectin on mast cells. We showed that ArtinM binds to mast cells, possibly to the high affinity receptor for immunoglobulin E (IgE) - FcεRI - and/or to IgE bound to FcεRI. Binding of the lectin resulted in protein tyrosine phosphorylation and release of the pre- and newly-formed mediators, β-hexosaminidase and LTB(4) by mast cells, activities that were potentiated in the presence of IgE. ArtinM also induced the activation of the transcription factors NFκB and NFAT, resulting in expression of some of their target genes such as IL-4 and TNF-α. In view of the established significance of mast cells in many immunological and inflammatory reactions, a better understanding of the mechanisms involved in mast cell activation by ArtinM ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473562</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473562</guid>        </item>
        <item>
            <title>Regulation of macrophage differentiation and polarization by group IVC phospholipase A(2).</title>
            <link>http://www.medworm.com/index.php?rid=5473561&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108055%26dopt%3DAbstract</link>
            <description>Authors: Ishihara K, Kuroda A, Sugihara K, Kanai S, Nabe T, Akiba S
    Abstract
    Although the cellular function of group IVC phospholipase A(2) (IVC-PLA(2)) remains to be understood, the expression of IVC-PLA(2) in human monocytic THP-1 cells was increased during phorbol ester-induced macrophage differentiation. We therefore examined the role of IVC-PLA(2) in macrophage differentiation using THP-1 cells. Two THP-1 cell lines stably expressing IVC-PLA(2)-specific shRNA were established. Differentiation and maturation into macrophages on treatment with phorbol ester were facilitated by knockdown of IVC-PLA(2) without the compensatory induction of mRNA expression for other group IV and VI PLA(2)s. Furthermore, the enhancement of macrophage differentiation by IVC-PLA(2)-knockdown were abol...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473561</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473561</guid>        </item>
        <item>
            <title>Extracellular low pH affects circadian rhythm expression in human primary fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5473560&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22115778%26dopt%3DAbstract</link>
            <description>Authors: Lee SK, Achieng E, Maddox C, Chen SC, Michael Iuvone P, Fukuhara C
    Abstract
    Circadian rhythm is a fundamental biological system involved in the regulation of various physiological functions. However, little is known about a nature or function of circadian clock in human primary cells. In the present study, we have applied in vitro real time circadian rhythm monitoring to study human clock properties using primary skin fibroblasts. Among factors that affect human physiology, slightly lower extracellular pH was chosen to test its effects on circadian rhythm expression. We established human primary fibroblast cultures obtained from three healthy subjects, stably delivered a circadian reporter gene Bmal1-luciferase, and recorded circadian rhythms in the culture medium at pH 7....</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473560</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473560</guid>        </item>
        <item>
            <title>NMR structure of human thymosin alpha-1.</title>
            <link>http://www.medworm.com/index.php?rid=5473559&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22115779%26dopt%3DAbstract</link>
            <description>Authors: Elizondo-Riojas MA, Chamow SM, Tuthill CW, Gorenstein DG, Volk DE
    Abstract
    800MHz NMR structure of the 28-residue peptide thymosin alpha-1 in 40% TFE/60% water (v/v) has been determined. Restrained molecular dynamic simulations with an explicit solvent box containing 40% TFE/60% TIP3P water (v/v) were used, in order to get the 3D model of the NMR structure. We found that the peptide adopts a structured conformation having two stable regions: an alpha-helix region from residues 14 to 26 and two double β-turns in the N-terminal twelve residues which form a distorted helical structure.
    PMID: 22115779 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473559</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473559</guid>        </item>
        <item>
            <title>Proteomics investigation of endogenous S-nitrosylation in Arabidopsis.</title>
            <link>http://www.medworm.com/index.php?rid=5473558&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22115780%26dopt%3DAbstract</link>
            <description>Authors: Fares A, Rossignol M, Peltier JB
    Abstract
    S-Nitrosylation emerges as an important protein modification in many processes. However, most data were obtained at the protein level after addition of a NO donor, particularly in plants where information about the cysteines nitrosylated in these proteins is scarce. An adapted work-flow, combining the classical biotin switch method and labeling with isotope-coded affinity tags (ICAT), is proposed. Without addition of NO donor, a total of 53 endogenous nitrosocysteines was identified in Arabidopsis cells, in proteins belonging to all cell territories, including membranes, and covering a large panel of functions. This first repertoire of nitrosothiols in plants enabled also preliminary structural description. Three apolar motifs, not...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473558</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473558</guid>        </item>
        <item>
            <title>3D structure and immunogenicity of Plasmodium falciparum sporozoite induced associated protein peptides as components of fully-protective anti-malarial vaccine.</title>
            <link>http://www.medworm.com/index.php?rid=5473556&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22115782%26dopt%3DAbstract</link>
            <description>Authors: Alba MP, Almonacid H, Calderón D, Chacón EA, Poloche LA, Patarroyo MA, Patarroyo ME
    Abstract
    SIAP-1 and SIAP-2 are proteins which are implicated in early events involving Plasmodium falciparum infection of the Anopheles mosquito vector and the human host. High affinity HeLa and HepG2 cell binding conserved peptides have been previously identified in these proteins, i.e. SIAP-1 34893 ((421)KVQGLSYLLRRKNGTKHPVY(440)) and SIAP-1 34899 ((541)YVLNSKLLNSRSFDKFKWIQ(560)) and SIAP-2 36879 ((181)LLLYSTNSEDNLDISFGELQ(200)). When amino acid sequences have been properly modified (replacements shown in bold) they have induced high antibody titres against sporozoites in Aotus monkeys (assessed by IFA) and in the corresponding recombinant proteins (determined by ELISA and Western blot)...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473556</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473556</guid>        </item>
        <item>
            <title>Lysosomal targeting of phafin1 mediated by Rab7 induces autophagosome formation.</title>
            <link>http://www.medworm.com/index.php?rid=5473555&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22115783%26dopt%3DAbstract</link>
            <description>We report here that the increased expression of phafin1 and its FYVE domain caused the formation of enlarged endosomes. Phafin1 also modulates the membrane density of certain receptors and participates in endocytosis and autophagy processes. The PH-domain of phafin1 is dispensable for lysosomal targeting. Moreover, the tail-domain of phafin1 provides lysosomal targeting signature and the ability to induce autophagy that is mediated by Rab7 signaling. The results suggest that in addition to its role in endosome transport, phafin1 is also involved in lysosomal targeting and autophagosome formation.
    PMID: 22115783 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473555</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473555</guid>        </item>
        <item>
            <title>CCCP induces autophagy in an AMPK-independent manner.</title>
            <link>http://www.medworm.com/index.php?rid=5473554&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22119190%26dopt%3DAbstract</link>
            <description>Authors: Kwon KY, Viollet B, Yoo OJ
    Abstract
    AMP-activated protein kinase (AMPK) is an important sensor of cellular energy status, and is involved in cell growth and autophagy through mammalian target of rapamycin complex 1 (mTORC1). Carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitochondrial uncoupler, leads to AMPK activation and Parkin-dependent mitophagy, respectively. However, the detailed biochemical mechanism of how CCCP induces autophagy or mitophagy has not been investigated yet. Here, we showed that CCCP inhibits mTORC1 independently of AMPK, although CCCP induces AMPK activation. Using wild type (WT) and AMPKα1/α2 double knockout (DKO) MEFs, we observed that CCCP promotes endogenous LC3 lipidation and formation of RFP-LC3 puncta, indicating autophagosome or autoly...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473554</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473554</guid>        </item>
        <item>
            <title>Towards understanding cell cycle control in Cryptococcus neoformans: Structure-function relationship of G1 and G1/S cyclins homologue CnCln1.</title>
            <link>http://www.medworm.com/index.php?rid=5473553&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22119191%26dopt%3DAbstract</link>
            <description>In this study, we investigated how CnCln1 cooperates with the cyclin-dependent kinases of S. cerevisiae (ScCdk1) and substitutes the function of G1 and G1/S cyclins of S. cerevisia from a point of view of their structure-function relationship. Our in silico analysis demonstrated that the CnCln1/ScCdk1 complex was more stable than any of the yeast cyclin and ScCdk1complexes. Thus, these results are consistent with in vitro analysis that has revealed the flexible functional capacity of CnCln1 as a Cdk1-related G1 and G1/S cyclins of S. cerevisiae.
    PMID: 22119191 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5473553</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5473553</guid>        </item>
        <item>
            <title>Two amino acids in each of D(1) and D(2) dopamine receptor cytoplasmic regions are involved in D(1)-D(2) heteromer formation.</title>
            <link>http://www.medworm.com/index.php?rid=5438024&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100647%26dopt%3DAbstract</link>
            <description>Authors: O'Dowd BF, Ji X, Nguyen T, George SR
    Abstract
    D(1) and D(2) dopamine receptors exist as heteromers in cells and brain tissue and are dynamically regulated and separated by agonist concentrations at the cell surface. We determined that these receptor pairs interact primarily through discrete amino acids in the cytoplasmic regions of each receptor, with no evidence of any D(1)-D(2) receptor transmembrane interaction found. Specifically involved in heteromer formation we identified, in intracellular loop 3 of the D(2) receptor, two adjacent arginine residues. Substitution of one of the arginine pair prevented heteromer formation. Also involved in heteromer formation we identified, in the carboxyl tail of the D(1) receptor, two adjacent glutamic acid residues. Substitution of ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438024</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438024</guid>        </item>
        <item>
            <title>New phenotypic aspects of the decidual spiral artery wall during early post-implantation mouse pregnancy.</title>
            <link>http://www.medworm.com/index.php?rid=5438020&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100651%26dopt%3DAbstract</link>
            <description>In conclusion, this study reveals novel aspects of the decidual SA muscular coat phenotype prior to and during early SAR that may have important implications for understanding the mechanisms of SAR.
    PMID: 22100651 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438020</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438020</guid>        </item>
        <item>
            <title>Increased cardiogenesis in P19-GFP teratocarcinoma cells expressing the propeptide IGF-1Ea.</title>
            <link>http://www.medworm.com/index.php?rid=5438019&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100652%26dopt%3DAbstract</link>
            <description>Authors: Poudel B, Bilbao D, Sarathchandra P, Germack R, Rosenthal N, Santini MP
    Abstract
    The mechanism implicated in differentiation of endogenous cardiac stem cells into cardiomyocytes to regenerate the heart tissue upon an insult remains elusive, limiting the therapeutical goals to exogenous cell injection and/or gene therapy. We have shown previously that cardiac specific overexpression of the insulin-like growth factor 1 propeptide IGF-1Ea induces beneficial myocardial repair after infarct. Although the mechanism is still under investigation, the possibility that this propeptide may be involved in promoting stem cell differentiation into the cardiac lineage has yet to be explored. To investigate whether IGF-1Ea promote cardiogenesis, we initially modified P19 embryonal carcino...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438019</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438019</guid>        </item>
        <item>
            <title>Ubiquitination of Notch1 is regulated by MAML1-mediated p300 acetylation of Notch1.</title>
            <link>http://www.medworm.com/index.php?rid=5438013&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100894%26dopt%3DAbstract</link>
            <description>In this study, we show that p300 acetylates Notch1 ICD in cell culture assay and in vitro, and conserved lysines located within the Notch C-terminal nuclear localization signal are essential for Notch acetylation. MAML1 and CSL, which are components of the Notch transcription complex, enhance Notch acetylation and we suggest that MAML1 increases Notch acetylation by potentiating p300 autoacetylation. Furthermore, MAML1-dependent acetylation of Notch1 ICD by p300 decreases the ubiquitination of Notch1 ICD in cellular assays. CDK8 has been shown to target Notch1 for ubiquitination and proteosomal degradation. We show that CDK8 inhibits Notch acetylation and Notch transcription enhanced by p300. Therefore, we speculate that acetylation of Notch1 might be a mechanism to regulate Notch activity...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438013</comments>
            <pubDate>Sat, 12 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438013</guid>        </item>
        <item>
            <title>Involvement of leucine zipper transcription factor-like protein 1 (Lztfl1) in the attenuation of cognitive impairment by exercise training.</title>
            <link>http://www.medworm.com/index.php?rid=5438036&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093827%26dopt%3DAbstract</link>
            <description>Authors: Sakurai T, Ogasawara J, Kizaki T, Ishibashi Y, Fujiwara T, Akagawa K, Izawa T, Oh-Ishi S, Haga S, Ohno H
    Abstract
    It is well known that exercise prevents and reduces cognitive impairment. In the present study, we focused on exercise training as a tool to prevent cognitive impairment, and searched for novel molecules that may relate to the prevention of cognitive impairment in the hippocampus. Two-month-old senescence-accelerated mouse prone-8 (SAMP8) mice were subjected to voluntary exercise training by running on a wheel for 4months, and were then assigned a conditioned fear memory test. Moreover, various mRNA levels in the hippocampus were examined by DNA array analysis and real-time PCR. Contextual fear memory in SAMP8 control mice was significantly impaired compared wi...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438036</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438036</guid>        </item>
        <item>
            <title>Role of suppressor of cytokine signaling 3 in lipid metabolism: Analysis based on a phage-display human liver cDNA library.</title>
            <link>http://www.medworm.com/index.php?rid=5438030&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093833%26dopt%3DAbstract</link>
            <description>In conclusion, SOCS3 is an important factor for lipid metabolism and a potential drug-target for treatment of widespread obesity.
    PMID: 22093833 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438030</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438030</guid>        </item>
        <item>
            <title>Involvement of the mitochondrial compartment in human NCL fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5438025&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100646%26dopt%3DAbstract</link>
            <description>In conclusion, the mitochondrial compartment is affected in NCL fibroblasts invitro, and CLN1 cells seem to be more vulnerable to the negative effects of stressed mitochondrial membrane than CLN6 cells.
    PMID: 22100646 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438025</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438025</guid>        </item>
        <item>
            <title>Rickettsia conorii infection stimulates the expression of ISG15 and ISG15 protease UBP43 in human microvascular endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5438023&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100648%26dopt%3DAbstract</link>
            <description>Authors: Colonne PM, Sahni A, Sahni SK
    Abstract
    Rickettsia conorii, an obligate intracellular bacterium and the causative agent of Mediterranean spotted fever, preferentially infects microvascular endothelial cells of the mammalian hosts leading to onset of innate immune responses, characterized by the activation of intracellular signaling mechanisms, release of pro-inflammatory cytokines and chemokines, and killing of intracellular rickettsiae. Our recent studies have shown that interferon (IFN)-β, a cytokine traditionally considered to be involved in antiviral immunity, plays an important role in the autocrine/paracrine regulation of host defense mechanism and control of R. conorii growth in the host endothelial cells. Here, we show that R. conorii infection induces the expressi...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438023</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438023</guid>        </item>
        <item>
            <title>Dynamic behavior of small heat shock protein inhibition on amyloid fibrillization of a small peptide (SSTSAA) from RNase A.</title>
            <link>http://www.medworm.com/index.php?rid=5438022&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100649%26dopt%3DAbstract</link>
            <description>Authors: Xi D, Dong X, Deng W, Lai L
    Abstract
    Small heat shock proteins, a class of molecular chaperones, are reported to inhibit amyloid fibril formation in vitro, while the mechanism of inhibition remains unknown. In the present study, we investigated the mechanism by which Mj HSP16.5 inhibits amyloid fibril formation of a small peptide (SSTSAA) from RNase A. A model peptide (dansyl-SSTSAA-W) was designed by introducing a pair of fluorescence resonance energy transfer (FRET) probes into the peptide, allowing for the monitoring of fibril formation by this experimental model. Mj HSP16.5 completely inhibited fibril formation of the model peptide at a molar ratio of 1:120. The dynamic process of fibril formation, revealed by FRET, circular dichroism, and electron microscopy, showed a...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438022</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438022</guid>        </item>
        <item>
            <title>Structure and dimerization of translation initiation factor aIF5B in solution.</title>
            <link>http://www.medworm.com/index.php?rid=5438021&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100650%26dopt%3DAbstract</link>
            <description>Authors: Rasmussen LC, Oliveira CL, Byron O, Jensen JM, Pedersen JS, Sperling-Petersen HU, Mortensen KK
    Abstract
    Translation initiation factor 5B (IF5B) is required for initiation of protein synthesis. The solution structure of archaeal IF5B (aIF5B) was analysed by small-angle X-ray scattering (SAXS) and dynamic light scattering (DLS) and was indicated to be in both monomeric and dimeric form. Sedimentation equilibrium (SE) analytical ultracentrifugation (AUC) of aIF5B indicated that aIF5B forms irreversible dimers in solution but only to a maximum of 5.0-6.8% dimer. Sedimentation velocity (SV) AUC at higher speed also indicated the presence of two species, and the sedimentation coefficients s(20,w)(0) were determined to be 3.64 and 5.51±0.29S for monomer and dimer, respectively. ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438021</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438021</guid>        </item>
        <item>
            <title>Suppression of phospholipase Cγ1 phosphorylation by cinnamaldehyde inhibits antigen-induced extracellular calcium influx and degranulation in mucosal mast cells.</title>
            <link>http://www.medworm.com/index.php?rid=5438018&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100653%26dopt%3DAbstract</link>
            <description>Authors: Kageyama-Yahara N, Wang X, Katagiri T, Wang P, Yamamoto T, Tominaga M, Kadowaki M
    Abstract
    Antigen-IgE-mediated mucosal mast-cell activation is critical in the development of food allergies. Cinnamaldehyde, a major constituent of Cinnamomi cortex, dose-dependently inhibited the antigen-IgE-induced degranulation of mucosal-type bone-marrow derived mast cells (mBMMCs) and RBL-2H3 cells. Cinnamaldehyde also suppressed the elevation of the intracellular Ca(2+) level that is induced by the extracellular Ca(2+) influx in antigen-IgE-stimulated mBMMCs. Furthermore, tyrosine phosphorylation of phospholipase C (PLC) γ1, which is a crucial activation switch for the intracellular Ca(2+) mobilization in mast cells, was attenuated by cinnamaldehyde. Together, our results demonstrated ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438018</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438018</guid>        </item>
        <item>
            <title>Regulation of miR-200c by nuclear receptors PPARα, LRH-1 and SHP.</title>
            <link>http://www.medworm.com/index.php?rid=5438017&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100809%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Yang Z, Whitby R, Wang L
    Abstract
    We investigated regulation of miR-200c expression by nuclear receptors. Ectopic expression of miR-200c inhibited MHCC97H cell migration, which was abrogated by the synergistic effects of PPARα and LRH-1 siRNAs. The expression of miR-200c was decreased by PPARα/LRH-1 siRNAs and increased by SHP siRNAs, and overexpression of the receptors reversed the effects of their respective siRNAs. SHP siRNAs also drastically enhanced the ability of the LRH-1 agonist RJW100 to induce miR-200c and downregulate ZEB1 and ZEB2 proteins. Co-expression of PPARα and LRH-1 moderately transactivated the miR-200c promoter, which was repressed by SHP co-expression. RJW100 caused strong activation of the miR-200c promoter. This is the first report to de...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438017</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438017</guid>        </item>
        <item>
            <title>Premutation huntingtin allele adopts a non-B conformation and contains a hot spot for DNA damage.</title>
            <link>http://www.medworm.com/index.php?rid=5438016&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100810%26dopt%3DAbstract</link>
            <description>Authors: Jarem DA, Delaney S
    Abstract
    The expansion of a CAG trinucleotide repeat (TNR) sequence has been linked to several neurological disorders, for example, Huntington's disease (HD). Healthy individuals have 5-35 CAG repeats. Those with 36-39 repeats have the premutation allele, which is known to be prone to expansion. In the disease state, greater than 40 repeats are present. Interestingly, the formation of non-B DNA conformations by the TNR sequence is proposed to contribute to the expansion. Here we provide the first structural and thermodynamic analysis of a premutation length TNR sequence. Using chemical probes of nucleobase accessibility, we found that similar to (CAG)(10), the premutation length sequence (CAG)(36) forms a stem-loop hairpin and contains a hot spot for DN...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438016</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438016</guid>        </item>
        <item>
            <title>Effects of a human plasma membrane-associated sialidase siRNA on prostate cancer invasion.</title>
            <link>http://www.medworm.com/index.php?rid=5438044&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093819%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effects and molecular mechanisms of Neu3 on cell invasion and migration in vivo and in vitro. Initially, we found that the levels of Neu3 expression were higher in prostate cancer tissues and cell lines than in normal prostate tissues based on RT-PCR and Western blotting analyses. We then applied a Neu3 siRNA approach to block Neu3 signaling using PC-3M cells as model cells. Transwell invasion assays and wound assays showed significantly decreased invasion and migration potential in the Neu3 siRNA-transfected cells. RT-PCR and Western blotting analyses revealed that Neu3 knockdown decreased the expressions of the matrix metalloproteinases MMP-2 and MMP-9. In vivo, mice injected with PC-3M cell tumors were evaluated by SPECT/CT to determine the presence of...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438044</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438044</guid>        </item>
        <item>
            <title>Expression and characterization of recombinant kurtoxin, an inhibitor of T-type voltage-gated calcium channels.</title>
            <link>http://www.medworm.com/index.php?rid=5438043&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093820%26dopt%3DAbstract</link>
            <description>Authors: Lee CW, Eu YJ, Min HJ, Cho EM, Lee JH, Kim HH, Nah SY, Swartz KJ, Kim JI
    Abstract
    Kurtoxin, a 63-amino acid peptide stabilized by four disulfide bonds, is the first reported peptide inhibitor of T-type voltage-gated calcium channels. Although T-type calcium channels have been implicated in a number of disease states, including epilepsy, chronic pain, hypertension and cancer, the lack of selective inhibitors has slowed progress in understanding their precise roles. Kurtoxin is a potentially valuable tool with which to study T-type calcium channels. However, because of the limited availability of the native protein, little is known about the structure and molecular mechanism of kurtoxin. Here we report the expression of kurtoxin in Escherichia coli and the structural and fun...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438043</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438043</guid>        </item>
        <item>
            <title>Use of human hepatocyte-like cells derived from induced pluripotent stem cells as a model for hepatocytes in hepatitis C virus infection.</title>
            <link>http://www.medworm.com/index.php?rid=5438042&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093821%26dopt%3DAbstract</link>
            <description>Authors: Yoshida T, Takayama K, Kondoh M, Sakurai F, Tani H, Sakamoto N, Matsuura Y, Mizuguchi H, Yagi K
    Abstract
    Host tropism of hepatitis C virus (HCV) is limited to human and chimpanzee. HCV infection has never been fully understood because there are few conventional models for HCV infection. Human induced pluripotent stem cell-derived hepatocyte-like (iPS-Hep) cells have been expected to use for drug discovery to predict therapeutic activities and side effects of compounds during the drug discovery process. However, the suitability of iPS-Hep cells as an experimental model for HCV research is not known. Here, we investigated the entry and genomic replication of HCV in iPS-Hep cells by using HCV pseudotype virus (HCVpv) and HCV subgenomic replicons, respectively. We showed that ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438042</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438042</guid>        </item>
        <item>
            <title>Preparation and characterization of cobalt-substituted anthrax lethal factor.</title>
            <link>http://www.medworm.com/index.php?rid=5438041&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093822%26dopt%3DAbstract</link>
            <description>Authors: Säbel CE, Carbone R, Dabous JR, Lo SY, Siemann S
    Abstract
    Anthrax lethal factor (LF) is zinc-dependent endopeptidase involved in the cleavage of mitogen-activated protein kinases near their N-termini. The current report concerns the preparation of cobalt-substituted LF (CoLF) and its characterization by electronic spectroscopy. Two strategies to produce CoLF were explored, including (i) a bio-assimilation approach involving the cultivation of LF-expressing Bacillus megaterium cells in the presence of CoCl(2), and (ii) direct exchange by treatment of zinc-LF with CoCl(2). Independent of the method employed, the protein was found to contain one Co(2+) per LF molecule, and was shown to be twice as active as its native zinc counterpart. The electronic spectrum of CoLF suggest...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438041</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438041</guid>        </item>
        <item>
            <title>Mode of ATM-dependent suppression of chromosome translocation.</title>
            <link>http://www.medworm.com/index.php?rid=5438040&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093823%26dopt%3DAbstract</link>
            <description>Authors: Yamauchi M, Suzuki K, Oka Y, Suzuki M, Kondo H, Yamashita S
    Abstract
    It is well documented that deficiency in ataxia telangiectasia mutated (ATM) protein leads to elevated frequency of chromosome translocation, however, it remains poorly understood how ATM suppresses translocation frequency. In the present study, we addressed the mechanism of ATM-dependent suppression of translocation frequency. To know frequency of translocation events in a whole genome at once, we performed centromere/telomere FISH and scored dicentric chromosomes, because dicentric and translocation occur with equal frequency and by identical mechanism. By centromere/telomere FISH analysis, we confirmed that chemical inhibition or RNAi-mediated knockdown of ATM causes 2 to 2.5-fold increase in dicentric...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438040</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438040</guid>        </item>
        <item>
            <title>5'-AMP-activated protein kinase (AMPK) regulates progesterone receptor transcriptional activity in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5438039&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093824%26dopt%3DAbstract</link>
            <description>Authors: Wu L, Huang XJ, Yang CH, Deng SS, Qian M, Zang Y, Li J
    Abstract
    The steroid hormone progesterone is an essential regulator of the cellular processes that are required for the development and maintenance of reproductive function. The diverse effects of progesterone are mediated by the progesterone receptor (PR). The functions of the PR are regulated not only by ligands but also by modulators of various cell signaling pathways. However, it is not clear which energy state regulates PR activity. AMP-activated protein kinase (AMPK), a serine/threonine protein kinase, is a key modulator of energy homeostasis. Once activated by an increasing cellular AMP:ATP ratio, AMPK switches off ATP-consuming processes and switches on ATP-producing processes. We found that both 5-aminoimidazo...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438039</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438039</guid>        </item>
        <item>
            <title>Expression of the prion-like protein Shadoo in the developing mouse embryo.</title>
            <link>http://www.medworm.com/index.php?rid=5438038&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093825%26dopt%3DAbstract</link>
            <description>Authors: Young R, Bouet S, Polyte J, Le Guillou S, Passet B, Vilotte M, Castille J, Beringue V, Le Provost F, Laude H, Vilotte JL
    Abstract
    The prion-like protein Shadoo has been suggested to compensate for the lack of PrP in Prnp-knockout mice, explaining their lack of extreme phenotype. In adult mice, both PrP and Shadoo have shown overlapping expression patterns and shared functions [1]. Their expression in the mouse embryo has also been suggested to be complementary, as invalidation of both genes results in embryonic lethality [2]. The developmental expression profile of PrP has been described from post-implantation stages up until birth [3-5]. However the spatial expression pattern of Shadoo in the developing mouse embryo is not known. We previously described the expression pro...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438038</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438038</guid>        </item>
        <item>
            <title>Transgenic overexpression of bone morphogenetic protein 11 propeptide in skeleton enhances bone formation.</title>
            <link>http://www.medworm.com/index.php?rid=5438037&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093826%26dopt%3DAbstract</link>
            <description>Authors: Li Z, Zeng F, Mitchell A, Kim YS, Wu Z, Yang J
    Abstract
    Bone morphogenetic protein 11 (BMP11) is a key regulatory protein in skeletal development. BMP11 propeptide has been shown to antagonize GDF11 activity in vitro. To explore the role of BMP11 propeptide in skeletal formation in vivo, we generated transgenic mice with skeleton-specific overexpression of BMP11 propeptide cDNA. The mice showed a transformation of the seventh cervical vertebra into a thoracic vertebra in our previous report. Presently, further characterizations of the transgenic mice indicated that ossification in calvatia was dramatically enhanced in transgenic fetuses at 16.5dpc in comparison with their wild-type littermates. At 10weeks of age, bone mineral content and bone mineral density were significa...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438037</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438037</guid>        </item>
        <item>
            <title>Characterisation and comparison of the chicken H1 RNA polymerase III promoter for short hairpin RNA expression.</title>
            <link>http://www.medworm.com/index.php?rid=5438035&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093828%26dopt%3DAbstract</link>
            <description>Authors: Cummins DM, Tyack SG, Doran TJ
    Abstract
    The U6 and 7SK RNA polymerase III promoters are widely used in RNAi research for the expression of shRNAs. However, with their increasing use in vitro and in vivo, issues associated with cytotoxicity have become apparent with their use. Therefore, alternative promoters such as the weaker H1 promoter are becoming a popular choice. With interest in the chicken as a model organism, we aimed to identify and characterise the chicken H1 promoter for the expression of shRNAs for the purpose of RNAi. The chicken H1 promoter was isolated and sequence analysis identified conserved RNA polymerase III promoter elements. A shRNA expression cassette containing the chicken H1 promoter and shRNA targeting enhanced green fluorescent protein (EGFP) wa...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438035</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438035</guid>        </item>
        <item>
            <title>Crystal structure and thermostability of a putative α-glucosidase from Thermotoga neapolitana.</title>
            <link>http://www.medworm.com/index.php?rid=5438034&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093829%26dopt%3DAbstract</link>
            <description>This study will help us to understand the function of the putative glucosidase and the structural features that affect the thermostability of the protein.
    PMID: 22093829 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438034</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438034</guid>        </item>
        <item>
            <title>Gold nanoparticle-assisted delivery of small, highly structured RNA into the nuclei of human cells.</title>
            <link>http://www.medworm.com/index.php?rid=5438033&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093830%26dopt%3DAbstract</link>
            <description>Authors: Ryou SM, Kim JM, Yeom JH, Hyun S, Kim S, Han MS, Kim SW, Bae J, Rhee S, Lee K
    Abstract
    Previous studies have shown that functionalized gold nanoparticles (AuNPs) can be used as a general platform for loading and delivering DNA oligonucleotides and short hairpin RNA to living systems. Here, we report the ability of functionalized AuNP to deliver RNA aptamers into the nuclei of human cells. An in vitro-synthesized RNA aptamer specific to the β-catenin protein was delivered into the HepG2 human cell line more efficiently via functionalized AuNP than liposome-based delivery, and resulted in nearly complete inhibition of β-catenin binding to the p50 subunit of NF-κB in the nucleus. This inhibition led to repression of NF-κB p50-dependent transcription of CRP. Also, the β-c...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438033</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438033</guid>        </item>
        <item>
            <title>Nkx3.2-induced suppression of Runx2 is a crucial mediator of hypoxia-dependent maintenance of chondrocyte phenotypes.</title>
            <link>http://www.medworm.com/index.php?rid=5438032&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093831%26dopt%3DAbstract</link>
            <description>Authors: Kawato Y, Hirao M, Ebina K, Tamai N, Shi K, Hashimoto J, Yoshikawa H, Myoui A
    Abstract
    Hypoxia is a key factor in the maintenance of chondrocyte identity. However, crucial chondrogenic transcription factors in the Sox families are not activated in this phenomenon, indicating that other pathways are involved. Nkx3.2 is a well-known chondrogenic transcription factor induced by Sonic hedgehog (Shh); it suppresses a key osteogenic transcriptional factor, Runt-related transcription factor 2 (Runx2), to maintain the chondrogenic phenotype in mesenchymal lineages. The purpose of this study was to examine the function of Nkx3.2 in hypoxia-dependent maintenance of chondrocyte identity. C3H10T1/2 pluripotent mesenchymal cells were cultured with rh-BMP2 (300ng/ml) to induce chondroge...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438032</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438032</guid>        </item>
        <item>
            <title>Triptolide inhibits COX-2 expression by regulating mRNA stability in TNF-α-treated A549 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5438031&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093832%26dopt%3DAbstract</link>
            <description>Authors: Sun L, Zhang S, Jiang Z, Huang X, Wang T, Huang X, Li H, Zhang L
    Abstract
    Cyclooxygenase-2 (COX-2) over-expression is frequently associated with human non-small-cell lung cancer (NSCLC) and involved in tumor proliferation, invasion, angiogenesis and resistance to apoptosis. In the present study, the effects of triptolide on COX-2 expression in A549 cells were investigated and triptolide was found to inhibit TNF-α-induced COX-2 expression. In our further studies, it was found that triptolide decreased the half-life of COX-2 mRNA dramatically and that it inhibited 3'-untranslated region (3'-UTR) fluorescence reporter gene activity. Meanwhile, triptolide inhibited the HuR shuttling from nucleus to cytoplasm. After triptolide treatment, decreased COX-2 mRNA in pull-down exper...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438031</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438031</guid>        </item>
        <item>
            <title>miR-125b suppresses the proliferation and migration of osteosarcoma cells through down-regulation of STAT3.</title>
            <link>http://www.medworm.com/index.php?rid=5438029&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093834%26dopt%3DAbstract</link>
            <description>Authors: Liu LH, Li H, Li JP, Zhong H, Zhang HC, Chen J, Xiao T
    Abstract
    There is accumulating evidence that microRNAs are involved in multiple processes in development and tumor progression. Abnormally expressed miR-125b was found to play a fundamental role in several types of cancer; however, whether miR-125b participates in regulating the initiation and progress of osteosarcoma still remains unclear. Here we demonstrate that miR-125b is frequently down-regulated in osteosarcoma samples and human osteosarcoma cell lines. The ectopic restoration of miR-125b expression in human osteosarcoma cells suppresses proliferation and migration in vitro and inhibits tumor formation in vivo. We further identified signal transducer and activator of transcription 3 (STAT3) as the direct and fun...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438029</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438029</guid>        </item>
        <item>
            <title>Evaluation of a UCMK/dCK fusion enzyme for gemcitabine-mediated cytotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=5438028&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093835%26dopt%3DAbstract</link>
            <description>Authors: Johnson AJ, Brown MN, Black ME
    Abstract
    While gemcitabine (2'-2'-difluoro-2'-deoxycytidine, dFdC) displays wide-ranging antineoplastic activity as a single agent, variable response rates and poor intracellular metabolism often limit its clinical efficacy. In an effort to enhance dFdC cytotoxicity and help normalize response rates, we created a bifunctional fusion enzyme that combines the enzymatic activities of deoxycytidine kinase (dCK) and uridine/cytidine monophosphate kinase (UCMK) in a single polypeptide. Our goal was to evaluate whether the created fusion could induce beneficial, functional changes toward dFdC, expedite dFdC conversion to its active antimetabolites and consequently amplify cell dFdC sensitivity. While kinetic analyses revealed the UCMK/dCK fusion enz...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438028</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438028</guid>        </item>
        <item>
            <title>A structural model of the HIV-1 Rev-integrase complex: The molecular basis of integrase regulation by Rev.</title>
            <link>http://www.medworm.com/index.php?rid=5438027&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093836%26dopt%3DAbstract</link>
            <description>Authors: Benyamini H, Loyter A, Friedler A
    Abstract
    The HIV-1 Rev and integrase (IN) proteins control important functions in the viral life cycle. We have recently discovered that the interaction between these proteins results in inhibition of IN enzymatic activity. Peptides derived from the Rev and IN binding interfaces have a profound effect on IN catalytic activity: Peptides derived from Rev inhibit IN, while peptides derived from IN stimulate IN activity by inhibiting the Rev-IN interaction. This inhibition leads to multi integration, genomic instability and specific death of virus-infected cells. Here we used protein docking combined with refinement and energy function ranking to suggest a structural model for the Rev-IN complex. Our results indicate that a Rev monomer binds I...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438027</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438027</guid>        </item>
        <item>
            <title>Novel multi-component enzyme machinery in lactic acid bacteria catalyzing CC double bond migration useful for conjugated fatty acid synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=5438026&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22093837%26dopt%3DAbstract</link>
            <description>Authors: Kishino S, Park SB, Takeuchi M, Yokozeki K, Shimizu S, Ogawa J
    Abstract
    Linoleic acid isomerase was identified as a multi-component enzyme system that consists of three enzymes that exist in both the membrane and soluble fractions of Lactobacillus plantarum. One enzyme (CLA-HY) is present in the membrane fraction, while two enzymes (CLA-DH and CLA-DC) exist in the soluble fraction. Three Escherichia coli transformants expressing CLA-HY, CLA-DH, and CLA-DC were constructed. Conjugated linoleic acid (CLA) and 10-hydroxy-12-octadecenoic acid were generated from linoleic acid only when all these three E. coli transformants were used as catalysts simultaneously. CLA-HY catalyzed the hydration reaction, a part of linoleic acid isomerization, to produce 10-hydroxy-12-octadecenoic...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438026</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438026</guid>        </item>
        <item>
            <title>A novel mechanism for an old drug: Amphotericin B in the treatment of visceral leishmaniasis.</title>
            <link>http://www.medworm.com/index.php?rid=5438015&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100811%26dopt%3DAbstract</link>
            <description>Authors: Chattopadhyay A, Jafurulla M
    Abstract
    Visceral leishmaniasis (VL) is caused by various species of the genus Leishmania. Internalization of Leishmania into host cells is facilitated by a large number of receptors, and therefore no panacea is available for the treatment of leishmaniasis. We previously demonstrated the requirement of host membrane cholesterol in the entry of Leishmania into macrophages by cholesterol depletion using methyl-β-cyclodextrin (MβCD). We recently showed that leishmanial infection is inhibited upon sequestration of host membrane cholesterol using amphotericin B (AmB), considered as the best existing drug against VL. The reason for the antileishmanial activity of AmB is generally believed to be its ability to bind ergosterol in parasite membranes. ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438015</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438015</guid>        </item>
        <item>
            <title>Newly identified essential amino acid residues affecting Δ(8)-sphingolipid desaturase activity revealed by site-directed mutagenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5438014&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22100812%26dopt%3DAbstract</link>
            <description>Authors: Li SF, Song LY, Zhang GJ, Yin WB, Chen YH, Wang RR, Hu ZM
    Abstract
    In order to identify amino acid residues crucial for the enzymatic activity of Δ(8)-sphingolipid desaturases, a sequence comparison was performed among Δ(8)-sphingolipid desaturases and Δ(6)-fatty acid desaturases from various plants. In addition to the known conserved cytb(5) (cytochrome b(5)) HPGG motif and three conserved histidine boxes, they share additional 15 completely conserved residues. A series of site-directed mutants were generated using our previously isolated Δ(8)-sphingolipid desaturase gene from Brassica rapa to evaluate the importance of these residues to the enzyme function. The mutants were functionally characterized by heterologous expression in yeast, allowing the identification of...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438014</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438014</guid>        </item>
        <item>
            <title>Potent and selective inhibition of hepatitis C virus replication by novel phenanthridinone derivatives.</title>
            <link>http://www.medworm.com/index.php?rid=5416447&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22085716%26dopt%3DAbstract</link>
            <description>Authors: Salim MT, Aoyama H, Sugita K, Watashi K, Wakita T, Hamasaki T, Okamoto M, Urata Y, Hashimoto Y, Baba M
    Abstract
    A number of novel phenanthridinone derivatives were examined for their inhibitory effect on hepatitis C virus (HCV) replication in Huh-7 cells harboring self-replicating subgenomic viral RNA replicons with a luciferase reporter (LucNeo#2). The activity of compounds was further confirmed by inhibition of viral RNA copy number in different subgenomic and full-genomic replicon cells using real-time reverse transcription polymerase chain reaction. Among the compounds, 4-butyl-11-(1,1,1,3,3,3-hexafluoro-2-hydroxypropan-2-yl)-7-methoxy-[1,3]dioxolo[4,5-c]phenanthridin-5(4H)-one (HA-719) was found to be the most active with a 50% effective concentration of 0.063±0.010...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416447</comments>
            <pubDate>Wed, 09 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416447</guid>        </item>
        <item>
            <title>Breast cancer metastasis suppressor 1 (BRMS1) is destabilized by the Cul3-SPOP E3 ubiquitin ligase complex.</title>
            <link>http://www.medworm.com/index.php?rid=5416446&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22085717%26dopt%3DAbstract</link>
            <description>Authors: Kim B, Nam HJ, Pyo KE, Jang MJ, Kim IS, Kim D, Boo K, Lee SH, Yoon JB, Baek SH, Kim JH
    Abstract
    Breast cancer metastasis suppressor 1 (BRMS1) suppresses metastasis without affecting primary tumorigenesis. The regulatory mechanism of BRMS1 at the protein level has not been revealed until recently. Here, we found that cullin 3 (Cul3), a component of E3 ubiquitin ligase, is a new binding partner of BRMS1 and the interaction between BRMS1 and Cul3 is mediated by the SPOP adaptor protein. Intriguingly, BRMS1 turns out to be a potent substrate that is ubiquitinated by the Cul3-SPOP complex. Knockdown of SPOP increases the level of BRMS1 protein and represses the expression of BRMS1 repressive target genes such as OPN and uPA in breast cancer cells. These results suggest that the...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416446</comments>
            <pubDate>Wed, 09 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416446</guid>        </item>
        <item>
            <title>Inhibition of PCGF2 enhances granulocytic differentiation of acute promyelocytic leukemia cell line HL-60 via induction of HOXA7.</title>
            <link>http://www.medworm.com/index.php?rid=5416445&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22085718%26dopt%3DAbstract</link>
            <description>In conclusion, we report that PCGF2, a PRC1 gene, played a negative role in the granulocytic differentiation of human APL cells.
    PMID: 22085718 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416445</comments>
            <pubDate>Wed, 09 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416445</guid>        </item>
        <item>
            <title>Bradykinin receptor 2 extends inflammatory cell recruitment in a model of acute gouty arthritis.</title>
            <link>http://www.medworm.com/index.php?rid=5416456&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079285%26dopt%3DAbstract</link>
            <description>Authors: Shaw OM, Harper JL
    Abstract
    The aim of this study was determine the effect of bradykinin receptor antagonism on MSU crystal-induced chemokine production and leukocyte recruitment. Mice were injected intraperitoneally with monosodium urate (MSU) crystals±bradykinin B1- or B2 receptor antagonists, Des-Arg-HOE-140 and HOE-140, respectively. MSU crystal-induced chemokine production and leukocyte recruitment in the peritoneum were measured over 24h and B1 and B2 receptor expression on leukocytes and peritoneal membrane was determined by flow cytometry and fluorescence microscopy. Data analysis showed that only B2 receptor antagonism decreased monocyte and neutrophil infiltration 24h post MSU crystal administration. Decreased leukocyte infiltration was associated with reduced m...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416456</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416456</guid>        </item>
        <item>
            <title>5-Hydroxy-eicosapentaenoic acid is an endogenous GPR119 agonist and enhances glucose-dependent insulin secretion.</title>
            <link>http://www.medworm.com/index.php?rid=5416455&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079287%26dopt%3DAbstract</link>
            <description>Authors: Kogure R, Toyama K, Hiyamuta S, Kojima I, Takeda S
    Abstract
    GPR119 is one of the G-protein-coupled receptors expressed in pancreatic β-cells and intestinal endocrine cells. Since agonists to GPR119 stimulate glucose-dependent insulin secretion, GPR119 agonists are anticipated to promote anti-diabetic effects and control of glucose homeostasis. Here, we reported that an omega-3 unsaturated fatty acid metabolite, 5-hydroxy-eicosapentaenoic acid (5-HEPE), was a potent agonist for GPR119 and enhanced glucose-dependent insulin secretion. 5-HEPE stimulated cAMP accumulation in mouse MIN6 insulinoma cells and human HuTu80 intestinal adenocarcinoma cells. These effects were blunted by GPR119-specific siRNA. Recombinant GPR119 also responded to 5-HEPE as well as authentic agonists...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416455</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416455</guid>        </item>
        <item>
            <title>Quercetin inhibits amyloid fibrillation of bovine insulin and destabilizes preformed fibrils.</title>
            <link>http://www.medworm.com/index.php?rid=5416454&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079288%26dopt%3DAbstract</link>
            <description>Authors: Wang JB, Wang YM, Zeng CM
    Abstract
    Growing interest and research efforts have recently been focused on elucidating the molecular mechanism of amyloid formation and the screening of effective inhibitors to interrupt amyloid structures. In the present study, the anti-amyloidogenic effects of quercetin were investigated in vitro using bovine insulin as a model protein. The results demonstrated that quercetin dose-dependently inhibited amyloid formation of insulin. Moreover, quercetin destabilized the preformed insulin fibrils and transformed the fibrils into amorphous aggregates. Hemolysis was observed when human erythrocytes were co-incubated with insulin fibrils. Quercetin inhibited fibril-induced hemolysis in a dose-dependent manner. SDS-PAGE showed that insulin fibrils in...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416454</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416454</guid>        </item>
        <item>
            <title>Increased salt and drought tolerance by d-ononitol production in transgenic Arabidopsis thaliana.</title>
            <link>http://www.medworm.com/index.php?rid=5416453&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079289%26dopt%3DAbstract</link>
            <description>Authors: Ahn C, Park U, Park PB
    Abstract
    The methylation of myo-inositol forms O-methyl inositol (d-ononitol) when plants are under abiotic stress in a reaction catalyzed by myo-inositol methyltransferase (IMT). d-Ononitol can serve as an osmoprotectant that prevents water loss in plants. We isolated the IMT cDNA from Glycine max and found by RT-PCR analysis that GmIMT transcripts are induced by drought and salinity stress treatments in the leaves of soybean seedlings. We confirmed the protein product of GmIMT and its substrate using a recombinant system in E. coli. Transgenic Arabidopsis plants over-expressing GmIMT displayed improved tolerance to dehydration stress treatment and to a lesser extent high salinity stress treatment. These results indicate that GmIMT is functional in ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416453</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416453</guid>        </item>
        <item>
            <title>High density cultures of embryoid bodies enhanced cardiac differentiation of murine embryonic stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5416452&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079290%26dopt%3DAbstract</link>
            <description>Authors: Lee MY, Bozkulak EC, Schliffke S, Amos PJ, Ren Y, Ge X, Ehrlich BE, Qyang Y
    Abstract
    Murine embryonic stem cell (mESC)-derived cardiomyocytes represent a promising source of cells for use in the development of models for studying early cardiac development as well as cell-based therapies in postnatal pathologies. Here, we report a highly efficient cardiac differentiation system in which high density embryoid body (EB) cultures leads to a marked increase of cardiomyocytes production from multiple mESC lines without the addition of any cardiogenic growth factors. Our results show that high density EB cultures significantly increase the yield of functional cardiomyocytes, which express typical cardiac markers, exhibit normal rhythmic Ca(2+) transients, and respond to both β-a...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416452</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416452</guid>        </item>
        <item>
            <title>Saxs data analysis and modeling of tetravalent neutralizing antibody CD4-IgG2 -/+ HIV-1 gp120 revealed that first two gp120 bind to the same Fab arm.</title>
            <link>http://www.medworm.com/index.php?rid=5416451&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079291%26dopt%3DAbstract</link>
            <description>Authors: Rathore YS, Solanki AK, Dhoke RR, Ashish 
    Abstract
    This communication describes SAXS data based global structures of tetravalent antibody CD4-IgG2 and its dimeric to pentameric complexes with gp120s. Comparison of models brought forth that while the two CD4s grafted on each arm remain tightly packed in the unliganded antibody, they enable binding of first two gp120s preferentially to the same Fab arm in an asymmetric manner. Retention of residues in the CD4-Fab linker earlier reasoned to enable bi-fold collapse of gp120-bound soluble CD4, and observed asymmetry of the (CD4-IgG2)/(gp120)(2) complex suggest that encoded flexibility in CD4-Fab linker is a critical structure-function factor for this broad spectrum neutralizing antibody.
    PMID: 22079291 [PubMed - as supplied...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416451</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416451</guid>        </item>
        <item>
            <title>Store-operated calcium entry is present in HL-1 cardiomyocytes and contributes to resting calcium.</title>
            <link>http://www.medworm.com/index.php?rid=5416450&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079292%26dopt%3DAbstract</link>
            <description>We report for the first time that these cells express stromal interaction molecule 1 (STIM1) and the Ca(2+) release-activated Ca(2+) (CRAC) channel Orai1, which are essential components of the SOCE machinery. In addition, SOCE is tightly coupled to sarcoplasmic reticulum (SR)-Ca(2+) release in HL-1 cells, and such response was not impaired in the presence of voltage dependent Ca(2+) channels (L-type and T-type channels) or reverse mode Na(+)/Ca(2+) exchanger (NCX) inhibitors. We were able to abolish the SOCE response with known SOCE inhibitors (BTP-2 and SKF-96365) and by targeted knockdown of Orai1 with RNAi. In addition, knockdown of Orai1 resulted in lower baseline Ca(2+) and an attenuated response to thapsigargin (TG) and caffeine, indicating that SOCE may play a role in Ca(2+) homeost...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416450</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416450</guid>        </item>
        <item>
            <title>Protein prenylation: A new mode of host-pathogen interaction.</title>
            <link>http://www.medworm.com/index.php?rid=5416449&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079293%26dopt%3DAbstract</link>
            <description>Authors: Amaya M, Baranova A, van Hoek ML
    Abstract
    Post translational modifications are required for proteins to be fully functional. The three step process, prenylation, leads to farnesylation and geranylgeranylation, which increase the hydrophobicity of the prenylated protein for efficient anchoring into plasma membranes and/or organellar membranes. Prenylated proteins function in a number of signaling and regulatory pathways that are responsible for basic cell operations. Well characterized prenylated proteins include Ras, Rac and Rho. Recently, pathogenic prokaryotic proteins, such as SifA and AnkB, have been shown to be prenylated by eukaryotic host cell machinery, but their functions remain elusive. The identification of other bacterial proteins undergoing this type of host-d...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416449</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416449</guid>        </item>
        <item>
            <title>An epifluorescence microscopy method for generalized polarization imaging.</title>
            <link>http://www.medworm.com/index.php?rid=5416448&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22079294%26dopt%3DAbstract</link>
            <description>Authors: Hansen JS, Hélix-Nielsen C
    Abstract
    Generalized polarization (GP) microscopy represents an excellent tool to study lipid-lipid and lipid-protein interactions in situ and in vitro. Here, we present an efficient and cost effective method to perform GP microscopy using a standard light-emitting diode (LED) epifluorescence microscope equipped with a digital color camera.
    PMID: 22079294 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416448</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416448</guid>        </item>
        <item>
            <title>PRaTo: A web-tool to select optimal primer pairs for qPCR.</title>
            <link>http://www.medworm.com/index.php?rid=5416444&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086170%26dopt%3DAbstract</link>
            <description>Authors: Nonis A, Scortegagna M, Nonis A, Ruperti B
    Abstract
    An essential pre-requisite to perform sound quantitative real-time polymerase chain reaction (qPCR) assays is to design outstanding primer pairs. This means they must have a good efficiency and be not prone to produce multiple amplicons or primer dimer products. To circumvent these issues, several softwares are available to help primer design. Although satisfactory computer-aided primer design tools are available for standard PCR, less efforts were done to provide specific methods for selection of optimal primer pairs for qPCR. We have developed PRaTo a web-based tool that enables checking and ranking of primers pairs for their attitude to perform optimally and reliably when used in qPCR experiments. PRaTo is available at...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416444</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416444</guid>        </item>
        <item>
            <title>DNA-binding properties of Smc6, a core component of the Smc5-6 DNA repair complex.</title>
            <link>http://www.medworm.com/index.php?rid=5416438&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086171%26dopt%3DAbstract</link>
            <description>Authors: Roy MA, D'Amours D
    Abstract
    The Smc5-6 complex is an essential regulator of chromosome integrity and a key component of the DNA damage response. As an essential DNA repair factor, the Smc5-6 complex is expected to interact with DNA and/or chromatin during the execution of its functions. How the Smc6 protein promotes the binding of the Smc5-6 complex to DNA lesions is currently unknown. We show here that Smc6 is a strong DNA-binding protein with a clear preference for single-stranded DNA substrates. Importantly, Smc6 associates with DNA in the absence of other Smc5-6 complex components and its activity is modulated by nucleotides. Our results also show that the minimal size of single-stranded DNA required for tight association with Smc6 is ∼60 nucleotides in length. Taken...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416438</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416438</guid>        </item>
        <item>
            <title>Functional characterization of a synthetic abscisic acid analog with anti-inflammatory activity on human granulocytes and monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=5416351&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086172%26dopt%3DAbstract</link>
            <description>Authors: Grozio A, Millo E, Guida L, Vigliarolo T, Bellotti M, Salis A, Fresia C, Sturla L, Magnone M, Galatini A, Damonte G, De Flora A, Bruzzone S, Bagnasco L, Zocchi E
    Abstract
    The phytohormone abscisic acid (ABA), in addition to regulating several important physiological functions in plants, is also produced and released by human granulocytes and monocytes where it stimulates cell activities involved in the innate immune response. Here we describe the properties of an ABA synthetic analog that competes with the hormone for binding to human granulocyte membranes and to purified recombinant LANCL2 (the human ABA receptor) and inhibits several ABA-triggered inflammatory functions of granulocytes and monocytes in vitro: chemotaxis, phagocytosis, reactive oxygen species production a...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416351</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416351</guid>        </item>
        <item>
            <title>A fluorescence assay for elucidating the substrate specificities of deubiquitinating enzymes.</title>
            <link>http://www.medworm.com/index.php?rid=5416109&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086173%26dopt%3DAbstract</link>
            <description>Authors: Yin ST, Huang H, Zhang YH, Zhou ZR, Song AX, Hong FS, Hu HY
    Abstract
    Ubiquitin C-terminal hydrolases (UCHs) are a representative family of deubiquitinating enzymes (DUBs), which specifically cleave ubiquitin (Ub) chains or extensions. Here we present a convenient method for characterizing the substrate specificities of various UCHs by fluorescently mutated Ub-fusion proteins (Ub(F45W)-Xaa) and di-ubiquitin chains (Ub(F45W)-diUb). After removal of the intact substrate by Ni(2+)-NTA affinity, the enzymatic activities of UCHs were quantitatively determined by recording fluorescence of the Ub(F45W) product. The results show that three UCHs, i.e. UCH-L1, UCH-L3 and UCH37/UCH-L5, are distinct in their substrate specificities for the Ub-fusions and diUb chains. This assay method ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416109</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416109</guid>        </item>
        <item>
            <title>Expression of membrane-bound NPP-type ecto-phosphodiesterases in rat podocytes cultured at normal and high glucose concentrations.</title>
            <link>http://www.medworm.com/index.php?rid=5416108&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086174%26dopt%3DAbstract</link>
            <description>In conclusion, ecto-nucleotide pyrophosphatase/phosphodiesterase 1 and 3 are expressed on podocytes, but changes in expression of these enzymes are most likely not involved in etiology of insulin resistance in podocytes.
    PMID: 22086174 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416108</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416108</guid>        </item>
        <item>
            <title>Identification of reference genes for reverse transcription quantitative real-time PCR normalization in pepper (Capsicum annuum L.).</title>
            <link>http://www.medworm.com/index.php?rid=5416107&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086175%26dopt%3DAbstract</link>
            <description>Authors: Wan H, Yuan W, Ruan M, Ye Q, Wang R, Li Z, Zhou G, Yao Z, Zhao J, Liu S, Yang Y
    Abstract
    Reverse transcription quantitative real-time polymerase chain reaction (qRT-PCR) is a commonly used technology for gene expression and transcriptome analysis. Normalization is a process that is necessary to accurately analyze qRT-PCR data. Stability of reference gene expression is required for this process. Due to the large variation in expression levels of reference genes obtained from different experimental conditions, gene expression stabilities must be evaluated and identified in all experimental systems. In the present paper, the stability of the expression levels of seven potential reference genes in pepper are assessed using qRT-PCR analysis to determine optimal reference genes....</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416107</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416107</guid>        </item>
        <item>
            <title>Basophil-derived mouse mast cell protease 11 induces microvascular leakage and tissue edema in a mast cell-independent manner.</title>
            <link>http://www.medworm.com/index.php?rid=5416106&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086176%26dopt%3DAbstract</link>
            <description>Authors: Yamagishi H, Mochizuki Y, Hamakubo T, Obata K, Ugajin T, Sato S, Kawano Y, Minegishi Y, Karasuyama H
    Abstract
    Mouse mast cell protease 11 (mMCP-11) is the most recently identified member of the mouse mast cell tryptase family. This tryptase is preferentially produced by basophils in contrast to other members that are expressed by mast cells but not basophils. Although blood-circulating basophils have long been considered as minor and redundant relatives of tissue-resident mast cells, recent studies illustrated that basophils and mast cells play distinct roles in vivo. To explore the in vivo role of basophil-derived mMCP-11, here we prepared recombinant mMCP-11 and its protease-dead mutant. Subcutaneous injection of the wild-type mMCP-11 but not the mutant induced edematous...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416106</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416106</guid>        </item>
        <item>
            <title>Suppression of Nrdp1 toxicity by Parkin in Drosophila models.</title>
            <link>http://www.medworm.com/index.php?rid=5416105&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086177%26dopt%3DAbstract</link>
            <description>Authors: Tan Y, Yu F, Pereira A, Morin P, Zhou J
    Abstract
    Nrdp1 is a RING finger ubiquitin E3 ligase that interacts with Parkin, and promotes the degradation of Parkin, a causative protein for early onset Autosomal Recessive Juvenile Parkinsonism (AR-JP). To investigate if Nrdp1 plays a role in the pathogenesis of Parkinson's disease, we generated transgenic Drosophila that expressed Drosophila Nrdp1 (dNrdp1) and dNrdp1(D56V), an aspartic acid to valine mutant at residue 56 that disrupts its ring finger domain, resulting in impaired capacity to degrade its substrate ErbB3. Our data show that a pan-neuronal expression of transgenic dNrdp1 but not dNrdp1(D56V) mutant leads to the loss of dopaminergic neurons in brains, resulting in reduction of dopamine production. These flies also m...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416105</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416105</guid>        </item>
        <item>
            <title>Cdc20 mediates D-box-dependent degradation of Sp100.</title>
            <link>http://www.medworm.com/index.php?rid=5416104&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086178%26dopt%3DAbstract</link>
            <description>Authors: Wang R, Li KM, Zhou CH, Xue JL, Ji CN, Chen JZ
    Abstract
    Cdc20 is a co-activator of the anaphase-promoting complex/cyclosome (APC/C complex), which recruits substrates at particular phases of the cell cycle and mediates their degradation. Sp100 is a PML-NB scaffold protein, which localizes to nuclear particles during interphase and disperses from them during mitosis, participates in viral resistance, transcriptional regulation, and apoptosis. However, its metabolism during the cell cycle has not yet been fully characterized. We found a putative D-box in Sp100 using the Eukaryotic Linear Motif (ELM) predictor database. The putative D-box of Sp100 was verified by mutational analysis. Overexpression of Cdc20 resulted in decreased levels of both endogenous Sp100 protein and ove...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416104</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416104</guid>        </item>
        <item>
            <title>Methionine sulfoxide reductase A regulates cell growth through the p53-p21 pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5416103&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22086179%26dopt%3DAbstract</link>
            <description>Authors: Choi SH, Kim HY
    Abstract
    MsrA is an oxidoreductase that catalyzes the stereospecific reduction of methionine-S-sulfoxide to methionine. Although MsrA is well-characterized as an antioxidant and has been implicated in the aging process and cellular senescence, its roles in cell proliferation are poorly understood. Here, we report a critical role of MsrA in normal cell proliferation and describe the regulation mechanism of cell growth by this protein. Down-regulation of MsrA inhibited cell proliferation, but MsrA overexpression did not promote it. MsrA deficiency led to an increase in p21, a major cyclin-dependent kinase inhibitor, thereby causing cell cycle arrest at the G(2)/M stage. While protein levels of p53 were not altered upon MsrA deficiency, its acetylation level w...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5416103</comments>
            <pubDate>Sun, 06 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5416103</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +203 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5377994&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F10%252F13%252007.55%2522%255BMHDA%255D%253A%25222011%252F11%252F05%252014.00%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F10%252F13%252007.55%2522%255BEDAT%255D%29%29</link>
            <description>203 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/11/05PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5377994</comments>
            <pubDate>Sat, 05 Nov 2011 18:00:02 +0100</pubDate>
            <guid isPermaLink="false">5377994</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +130 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5294701&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F10%252F03%252004.04%2522%255BMHDA%255D%253A%25222011%252F10%252F08%252005.29%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F10%252F03%252004.04%2522%255BEDAT%255D%29%29</link>
            <description>130 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/10/08PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294701</comments>
            <pubDate>Sat, 08 Oct 2011 09:29:50 +0100</pubDate>
            <guid isPermaLink="false">5294701</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +232 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5274606&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F09%252F22%252020.59%2522%255BMHDA%255D%253A%25222011%252F10%252F03%252004.04%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F09%252F22%252020.59%2522%255BEDAT%255D%29%29</link>
            <description>232 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/10/03PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274606</comments>
            <pubDate>Mon, 03 Oct 2011 08:04:51 +0100</pubDate>
            <guid isPermaLink="false">5274606</guid>        </item>
        <item>
            <title>Enhanced sensitivity of A549 cells to the cytotoxic action of anticancer drugs via suppression of Nrf2 by procyanidins from Cinnamomi Cortex extract.</title>
            <link>http://www.medworm.com/index.php?rid=5244133&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925486%26dopt%3DAbstract</link>
            <description>Authors: Ohnuma T, Matsumoto T, Itoi A, Kawana A, Nishiyama T, Ogura K, Hiratsuka A
    Abstract
    Nuclear factor-E2-related factor 2 (Nrf2) is an important cytoprotective transcription factor because Nrf2-regulated enzymes play a key role in antioxidant and detoxification processes. Recent studies have reported that lung cancer cells overexpressing Nrf2 exhibit increased resistance to chemotherapy. Suppression of overexpressed Nrf2 is needed for a new therapeutic approach against lung cancers. In the present study, we found that Cinnamomi Cortex extract (CCE) has an ability to suppress Nrf2-regulated enzyme activity and Nrf2 expression in human lung cancer A549 cells with high Nrf2 activity. Moreover, we demonstrated that CCE significantly enhances sensitivity of A549 cells to the cytot...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244133</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244133</guid>        </item>
        <item>
            <title>Modulation of cytochrome P450 gene expression in primary hepatocytes on various artificial extracellular matrices.</title>
            <link>http://www.medworm.com/index.php?rid=5244132&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21930114%26dopt%3DAbstract</link>
            <description>Authors: Adachi T, Goto M, Cho CS, Akaike T
    Abstract
    We studied effect of artificial extracellular matrices (ECMs), such as collagen I, poly (N-p-vinylbenzyl-4-O-β-d-galactopyranosyl-d-gluconamide)(PVLA) and E-cadherin-IgG Fc (E-cad-Fc) on hepatic metabolism to identify the mechanism of in vivo hepatocellular functional and metabolic integrity. mRNA expression of liver function marker, cytochrome P450 (CYP) and transporter genes in hepatocytes were compared among used ECMs using real-time RT-PCR. mRNA expressions of Cyp2c29 and Cyp2d22 among CYP genes in hepatocytes on PVLA were recovered after 3days due to enhanced liver-specific function by the spheroid formation of hepatocytes whereas mRNA expressions of CYP genes in hepatocytes on collagen and E-cad-Fc drastically decreased wi...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244132</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244132</guid>        </item>
        <item>
            <title>Kinemage of action - Proposed reaction mechanism of glutamate-1-semialdehyde mutase at an atomic level.</title>
            <link>http://www.medworm.com/index.php?rid=5244131&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21930115%26dopt%3DAbstract</link>
            <description>Authors: Sorensen JL, Stetefeld J
    Abstract
    Glutamate-1-semialdehyde mutase (GSAM), a key enzyme in tetrapyrrole cofactor biosynthesis, performs a unique transamination on a single substrate. The substrate, glutamate-1-semialdehyde (GSA), undergoes a reaction that exchanges the position of an amine and a carbonyl group to produce 5-aminolevulinic acid (ALA). This transamination reaction is unique in the fact that is does not require an external cofactor to act as a nitrogen donor or acceptor in this transamination reaction. One of the other remarkable features of the catalytic mechanism is the release free in the enzyme active site of the intermediate 4,5-diaminovaleric acid (DAVA). The action of a gating loop prevents the escape of DAVA from the active site. In a MD simulation appr...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244131</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244131</guid>        </item>
        <item>
            <title>Oxidized low-density lipoprotein-induced periodontal inflammation is associated with the up-regulation of cyclooxygenase-2 and microsomal prostaglandin synthase 1 in human gingival epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=5244144&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925143%26dopt%3DAbstract</link>
            <description>In this study, the role of oxLDL in the gingival epithelial cell inflammatory response was further investigated using Ca9-22 cells and primary human oral keratinocytes (HOK). Treatment of Ca9-22 cells and HOK with oxLDL induced an up-regulation of IL-8 and the PGE(2)-producing enzymes, cyclooxygenase-2 and microsomal PGE(2) synthase-1. These responses induced by oxLDL were significantly suppressed by a nuclear factor-kappa B (NF-κB) inhibitor. However, unlike the result in macrophages, oxLDL did not lead to an increase in CD36 expression in these two cells. These results suggest that oxLDL elicits gingival epithelial cell inflammatory responses through an activation of the NF-κB pathway. These data suggest a mechanistic link between periodontal disease and lipid metabolism-related disord...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244144</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244144</guid>        </item>
        <item>
            <title>Differentiation of human umbilical cord mesenchymal stem cells into dermal fibroblasts in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5244143&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925144%26dopt%3DAbstract</link>
            <description>In this study, we collected newborn umbilical cord tissue under sterile conditions and isolated UCMSCs through a tissue attachment method. UCMSC cell surface markers were examined using flow cytometry. On the third passage, UCMSCs were induced to differentiate into dermal fibroblasts in conditioned induction media. The induction results were detected using immunofluorescence with a fibroblast-specific monoclonal antibody and real time PCR for type I and type III collagen. UCMSCs exhibited a fibroblast-like morphology and reached 90% confluency 14 to 18days after primary culture. Cultured UCMSCs showed strong positive staining for CD73, CD29, CD44, CD105, and HLA-I, but not CD34, CD45, CD31, or HLA-DR. After differentiation, immunostaining for collagen type I, type III, fibroblast-specific ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244143</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244143</guid>        </item>
        <item>
            <title>CTGF/CCN2 has a chemoattractive function but a weak adhesive property to embryonic carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5244141&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925146%26dopt%3DAbstract</link>
            <description>In conclusion, our findings support the chemoattractive role of CCN2 for P19 cells, but not its adhesive role when compared to laminin or fibronectin.
    PMID: 21925146 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244141</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244141</guid>        </item>
        <item>
            <title>Progress in demonstrating total homochiral selection in montmorillonite-catalyzed RNA synthesis.</title>
            <link>http://www.medworm.com/index.php?rid=5244140&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925147%26dopt%3DAbstract</link>
            <description>Authors: Joshi PC, Aldersley MF, Ferris JP
    Abstract
    The Na(+)-montmorillonite-catalyzed reactions of 5'-phosphorimidazolites of nucleosides generates RNA oligomers. The question arises as to how chiral selectivity was introduced into this biopolymer from a simple chemical system. We have demonstrated homochiral selection in quaternary reactions of a racemic mixture of d,l-ImpA and d,l-ImpU on Na(+)-montmorillonite. The dimer, trimer, tetramer and pentamer fractions were investigated for homochiral selection. The products were collected via ion exchange HPLC and their terminal 5'-phosphate was cleaved by alkaline phosphatase. These fractions were analyzed by reverse phase HPLC for the identification of homochiral and heterochiral isomers. Encouraged by favorable homochiral excesses ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244140</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244140</guid>        </item>
        <item>
            <title>Longistatin, a novel plasminogen activator from vector ticks, is resistant to plasminogen activator inhibitor-1.</title>
            <link>http://www.medworm.com/index.php?rid=5244137&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925150%26dopt%3DAbstract</link>
            <description>Authors: Anisuzzaman , Khyrul Islam M, Abdul Alim M, Miyoshi T, Hatta T, Yamaji K, Matsumoto Y, Fujisaki K, Tsuji N
    Abstract
    Thrombo-occlusive diseases are major causes of morbidity and mortality, and tissue-type plasminogen activator (t-PA) is recommended for the treatment of the maladies. However, both t-PA and u-PA are rapidly inactivated by plasminogen activator inhibitor-1 (PAI-1). Here, we show that longistatin, a novel plasminogen activator isolated from the ixodid tick, Haemaphysalis longicornis is resistant to PAI-1. Longistatin was relatively less susceptible to the inhibitory effect of SDS-treated platelet lysate than physiologic PAs. Platelet lysate inhibited t-PA and tcu-PA with the IC(50) of 7.7 and 9.1μg/ml, respectively, whereas for longistatin inhibition IC(50) wa...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244137</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244137</guid>        </item>
        <item>
            <title>Anti-Parkinsonian effects of Bacopa monnieri: Insights from transgenic and pharmacological Caenorhabditis elegans models of Parkinson's disease.</title>
            <link>http://www.medworm.com/index.php?rid=5244135&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925152%26dopt%3DAbstract</link>
            <description>Authors: Jadiya P, Khan A, Sammi SR, Kaur S, Mir SS, Nazir A
    Abstract
    Neurodegenerative Parkinson's disease (PD) is associated with aggregation of protein alpha synuclein and selective death of dopaminergic neurons, thereby leading to cognitive and motor impairment in patients. The disease has no complete cure yet; the current therapeutic strategies involve prescription of dopamine agonist drugs which turn ineffective after prolonged use. The present study utilized the powerful genetics of model system Caenorhabditis elegans towards exploring the anti-Parkinsonian effects of a neuro-protective botanical Bacopa monnieri. Two different strains of C. elegans; a transgenic model expressing &quot;human&quot; alpha synuclein [NL5901 (P(unc-54)::alphasynuclein::YFP+unc-119)], and a pharmacological ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244135</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244135</guid>        </item>
        <item>
            <title>Pilot analysis of the plasma metabolite profiles associated with emphysematous Chronic Obstructive Pulmonary Disease phenotype.</title>
            <link>http://www.medworm.com/index.php?rid=5244134&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925153%26dopt%3DAbstract</link>
            <description>Authors: Paige M, Burdick MD, Kim S, Xu J, Lee JK, Michael Shim Y
    Abstract
    The current pilot study examined the hypothesis that cigarette smokers who developed an emphysematous phenotype of Chronic Obstructive Pulmonary Disease (COPD) were associated with distinctive patterns in their corresponding metabolomics profile as compared to those who did not. Peripheral blood plasma samples were collected from 38 subjects with different phenotypes of COPD. They were categorized into three groups: healthy non-smokers (n=16), smokers without emphysema (n=8), and smokers with emphysema (n=14). Ultra High Performance Liquid Chromatography/quadrupole-Time-of-Flight Mass Spectrometry techniques were used to identify a large number of metabolite markers (3534). Unsupervised clustering analysis a...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244134</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244134</guid>        </item>
        <item>
            <title>Endosomal trafficking of the G protein-coupled receptor somatostatin receptor 3.</title>
            <link>http://www.medworm.com/index.php?rid=5244145&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925142%26dopt%3DAbstract</link>
            <description>Authors: Tower-Gilchrist C, Lee E, Sztul E
    Abstract
    Intracellular trafficking of G protein-coupled receptors (GPCRs) regulates their surface availability and determines cellular response to agonists. Rab GTPases regulate membrane trafficking and identifying Rab networks controlling GPCR trafficking is essential for understanding GPCR signaling. We used real time imaging to show that somatostatin receptor 3 (SSTR3) traffics through Rab4-, Rab21-, and Rab11-containing endosomes, but largely bypasses Rab5 and Rab7 endosomes. We show that SSTR3 rapidly traffics through Rab4 endosomes but moves slower through Rab21 and Rab11 endosomes. SSTR3 passage through each endosomal compartment is regulated by the cognate Rab since expression of the inactive Rab4/S22N, Rab21/T33N, and Rab11/S25N i...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244145</comments>
            <pubDate>Wed, 07 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244145</guid>        </item>
        <item>
            <title>A small unstructured nucleic acid disrupts a trinucleotide repeat hairpin.</title>
            <link>http://www.medworm.com/index.php?rid=5244152&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924238%26dopt%3DAbstract</link>
            <description>Authors: Avila-Figueroa A, Cattie D, Delaney S
    Abstract
    A variety of neurodegenerative disorders are associated with the expansion of trinucleotide repeat (TNR) sequences. These repetitive sequences are prone to adopting non-canonical structures, such as intrastrand stem-loop hairpins. Indeed, the formation and persistence of these hairpins during DNA replication and/or repair have been proposed as factors that facilitate TNR expansion. Given this proposed contribution of TNR hairpins to the expansion mechanism, disruption of such structures via strand invasion offers a potential means to negate the disease-initiating expansion. In this work, we investigated the strand invading abilities of a (CTG)(3) unstructured nucleic acid on a (CAG)(10) TNR hairpin. Using fluorescence, optical...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244152</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244152</guid>        </item>
        <item>
            <title>Comparing mechano-transduction in fibroblasts deficient of focal adhesion proteins.</title>
            <link>http://www.medworm.com/index.php?rid=5244151&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924239%26dopt%3DAbstract</link>
            <description>Authors: Dey T, Mann MC, Goldmann WH
    Abstract
    Mechano-transduction was studied in wildtype and focal adhesion (FA) protein-deficient mouse embryonic fibroblasts (MEFs). Using a cell stretcher, we determined the effect of stretch on cell morphology, apoptosis, and phosphorylation of ERK(1/2). After 20% cyclic, uniaxial stretch, FA-deficient MEFs showed morphological changes and levels of apoptosis of the order: focal adhesion kinase&amp;gt;p130Cas&amp;gt;vinculin compared to wildtype cells. ERK(1/2) phosphorylation peaked in wildtype cells at around 10min, and in all FA-deficient cells at around 5min. The relative change in strain energy of FA-deficient cells compared to wildtype cells was of the order: vinculin&amp;gt;FAK&amp;gt;p130Cas. Taken together, FAK and p130Cas are more important in the st...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244151</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244151</guid>        </item>
        <item>
            <title>Copper-mediated cross-linking of S100A4, but not of S100A2, results in proinflammatory effects in melanoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5244150&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924240%26dopt%3DAbstract</link>
            <description>Authors: Haase-Kohn C, Wolf S, Lenk J, Pietzsch J
    Abstract
    The aim of this study was to investigate the response to and the physiological consequences of copper-mediated cross-linking of S100A2 and S100A4, two members of the S100 family of EF-hand calcium-binding proteins. As demonstrated by electrophoresis and mass spectrometry techniques S100A2 and S100A4 show formation of cross-links due to copper-mediated oxidation of cysteine residues. For S100A4, but not for S100A2, this results in both increased activation of NFκB and secretion of TNF-α in human A375 and, to a higher extent, in RAGE-transfected melanoma cells. The data suggest that a prooxidative tumor microenvironment enhances proinflammatory and prometastatic action of S100A4.
    PMID: 21924240 [PubMed - as supplied by ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244150</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244150</guid>        </item>
        <item>
            <title>Function of yeast and amphioxus tRNA ligase in IRE1alpha-dependent XBP1 mRNA splicing.</title>
            <link>http://www.medworm.com/index.php?rid=5244149&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924241%26dopt%3DAbstract</link>
            <description>We examined whether yeast and amphioxus RNA ligases for tRNA splicing function in RNA ligation in mammalian XBP1 splicing. Both RNA ligases functioned in RNA ligation in mammalian XBP1 splicing in vitro. Interestingly, Clp1, and PNK/CPDase were not necessary for exon-exon ligation in XBP1 mRNA by amphioxus RNL. These results suggest that RNA ligase for tRNA splicing might therefore commonly function as an RNA ligase for XBP1 mRNA splicing.
    PMID: 21924241 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244149</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244149</guid>        </item>
        <item>
            <title>Exploring the activation mechanism of TRPM8 channel by targeted MD simulations.</title>
            <link>http://www.medworm.com/index.php?rid=5244148&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924242%26dopt%3DAbstract</link>
            <description>Authors: Pedretti A, Labozzetta A, Monte ML, Beccari AR, Moriconi A, Vistoli G
    Abstract
    The TRPM8 cation channel belongs to the superfamily of transient receptor potential (TRP). It is involved in non-painful cool sensation and is triggered by diverse chemical and physical stimuli whose precise activation mechanism is still unknown. The study presents a set of targeted molecular dynamics (MD) simulations involving selected complexes of the TRPM8 channel whose homology model was recently generated by some of us. More in detail, the MD simulations concerned the TRPM8 alone and in complex with agonists and antagonists. These simulations were focused on voltage sensor module and designed to validate the ligand induced activation mechanism as hypothesized in a previous study. The obtain...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244148</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244148</guid>        </item>
        <item>
            <title>Identification of three novel mutations in the COL2A1 gene in four unrelated Chinese families with spondyloepiphyseal dysplasia congenita.</title>
            <link>http://www.medworm.com/index.php?rid=5244147&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924244%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Our study extends the mutation spectrum of SEDC and is helpful in early molecular diagnoses of SEDC.
    PMID: 21924244 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244147</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244147</guid>        </item>
        <item>
            <title>Human CD1d molecules are resistant to human cytomegalovirus US2- and US11-mediated degradation.</title>
            <link>http://www.medworm.com/index.php?rid=5244146&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925141%26dopt%3DAbstract</link>
            <description>Authors: Cho S, Jun Y
    Abstract
    Natural killer T (NKT) cells may play a crucial role in controlling viral infection by bridging the innate and adaptive immune systems. These cells are activated by lipids presented by CD1d molecules, which are structurally homologous to major histocompatibility complex class I (MHC-I) molecules. Although human cytomegalovirus (HCMV) can avoid T cell recognition by down-regulating MHC-I-mediated antigen presentation, it remains unknown whether it can also interfere with CD1d-mediated lipid presentation. Here, we show that CD1d is resistant to rapid degradation induced by the HCMV gene products US2 and US11, which cause dislocation of MHC-I molecules from the endoplasmic reticulum (ER) to the cytosol for destruction by proteasomes. The resistance of CD...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244146</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244146</guid>        </item>
        <item>
            <title>Differential regulation of the SMN2 gene by individual HDAC proteins.</title>
            <link>http://www.medworm.com/index.php?rid=5244142&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925145%26dopt%3DAbstract</link>
            <description>Authors: Evans MC, Cherry JJ, Androphy EJ
    Abstract
    Spinal muscular atrophy (SMA) is an autosomal recessive neurodegenerative disorder that is the leading genetic cause of infantile death. SMA is caused by homozygous deletion or mutation of the survival of motor neuron 1 gene (SMN1). The SMN2 gene is nearly identical to SMN1, however is alternatively spliced. The close relationship to SMN1 results in SMN2 being a very power genetic modifier of SMA disease severity and a target for therapies. We sought to identify the regulatory role individual HDAC proteins use to control expression of full length protein from the SMN2 genes. We used quantitative PCR to determine the effects shRNA silencing of individual HDACs on the steady state levels of a SMN2-luciferase reporter transcripts. We ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244142</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244142</guid>        </item>
        <item>
            <title>Systematic selection of housekeeping genes for gene expression normalization in chicken embryo fibroblasts infected with Newcastle disease virus.</title>
            <link>http://www.medworm.com/index.php?rid=5244139&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925148%26dopt%3DAbstract</link>
            <description>Authors: Yin R, Liu X, Liu C, Ding Z, Zhang X, Tian F, Liu W, Yu J, Li L, de Angelis MH, Stoeger T
    Abstract
    Gene expression analysis frequently used to analyze the response to viral infection, and 18S RNA, SHDA and GAPDH represent popular house keeping genes (HKGs) often used to normalize gene expression. Here we describe the first systematic selection and evaluation of suitable HKGs for gene expression analysis in chicken embryo fibroblasts (CEF) infected with NDV adapted to the guidelines from Gorzelniak and Ferguson. Our results indicate that ACTB, HPRT1 and HMBS were valuable and stable HKGs, while 18S RNA, GAPDH and SHDA are considerably regulated during the course of infection and thus precluded for normalization. Normalizing the infection dependent gene IFN-a and the infecti...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244139</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244139</guid>        </item>
        <item>
            <title>Synthetic Fab fragments that bind the HIV-1 gp41 heptad repeat regions.</title>
            <link>http://www.medworm.com/index.php?rid=5244138&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925149%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Regula LK, Stewart A, Lai JR
    Abstract
    Recent work has demonstrated that antibody phage display libraries containing restricted diversity in the complementarity determining regions (CDRs) can be used to target a wide variety of antigens with high affinity and specificity. In the most extreme case, antibodies whose combining sites are comprised of only two residues - tyrosine and serine - have been identified against several protein antigens. [F.A. Fellouse, B. Li, D.M. Compaan, A.A. Peden, S.G. Hymowitz, S.S. Sidhu, J. Mol. Biol. 348 (2005) 1153-1162.] Here, we report the isolation and characterization of antigen-binding fragments (Fabs) from such &quot;minimalist&quot; diversity synthetic antibody libraries that bind the heptad repeat regions of human immunodeficiency virus t...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244138</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244138</guid>        </item>
        <item>
            <title>Hsp90α/β associates with the GSK3β/axin1/phospho-β-catenin complex in the human MCF-7 epithelial breast cancer model.</title>
            <link>http://www.medworm.com/index.php?rid=5244136&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21925151%26dopt%3DAbstract</link>
            <description>Authors: Cooper LC, Prinsloo E, Edkins AL, Blatch GL
    Abstract
    Hsp90α/β, the signal transduction chaperone, maintains intracellular communication in normal, stem, and cancer cells. The well characterised association of Hsp90α/β with its client kinases form the framework of multiple signalling networks. GSK3β, a known Hsp90α/β client, mediates β-catenin phosphorylation as part of a cytoplasmic destruction complex which targets phospho-β-catenin to the 26S proteasome. The canonical Wnt/β-catenin pathway promotes stem cell self-renewal as well as oncogenesis. The degree of Hsp90α/β involvement in Wnt/β-catenin signalling needs clarification. Here, we describe the association of Hsp90α/β with GSK3β, β-catenin, phospho-β-catenin and the molecular scaffold, axin1, in the...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5244136</comments>
            <pubDate>Tue, 06 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5244136</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +107 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5191909&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F08%252F29%252020.24%2522%255BMHDA%255D%253A%25222011%252F09%252F04%252001.20%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F08%252F29%252020.24%2522%255BEDAT%255D%29%29</link>
            <description>107 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/09/04PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5191909</comments>
            <pubDate>Sun, 04 Sep 2011 05:20:02 +0100</pubDate>
            <guid isPermaLink="false">5191909</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +131 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5140515&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F08%252F04%252020.45%2522%255BMHDA%255D%253A%25222011%252F08%252F19%252010.10%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F08%252F04%252020.45%2522%255BEDAT%255D%29%29</link>
            <description>131 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/08/19PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5140515</comments>
            <pubDate>Fri, 19 Aug 2011 14:10:02 +0100</pubDate>
            <guid isPermaLink="false">5140515</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +218 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5094944&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F07%252F21%252014.00%2522%255BMHDA%255D%253A%25222011%252F08%252F04%252020.45%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F07%252F21%252014.00%2522%255BEDAT%255D%29%29</link>
            <description>218 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/08/04PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5094944</comments>
            <pubDate>Fri, 05 Aug 2011 00:45:07 +0100</pubDate>
            <guid isPermaLink="false">5094944</guid>        </item>
        <item>
            <title>&quot;Biochem Biophys Res Commun&quot;; +148 new citations</title>
            <link>http://www.medworm.com/index.php?rid=5043543&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fsites%2Fentrez%3Fcmd%3DSearch%26db%3Dpubmed%26term%3D%28%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%29%2520AND%2520%25222011%252F07%252F06%252005.00%2522%255BMHDA%255D%253A%25222011%252F07%252F21%252014.00%2522%255BMHDA%255D%29%29%2520NOT%2520%28%28%2520%28%28%2522Biochem%2520Biophys%2520Res%2520Commun%2522%255BTIAB%255D%29%29%2520AND%2520%25220001%2522%255BEDAT%255D%253A%25222011%252F07%252F06%252005.00%2522%255BEDAT%255D%29%29</link>
            <description>148 new pubmed citations were retrieved for your search.
Click on the search hyperlink below to display the complete search results:

&quot;Biochem Biophys Res Commun&quot;
These pubmed results were generated on 2011/07/21PubMed, a service of the National Library of Medicine, includes over 15 million 
citations for biomedical articles back to the 1950's.
These citations are from MEDLINE and additional life science journals. 
PubMed includes links to many sites providing full text articles and other related resources. (Source: Biochemical and Biophysical Research communications)</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5043543</comments>
            <pubDate>Thu, 21 Jul 2011 18:00:02 +0100</pubDate>
            <guid isPermaLink="false">5043543</guid>        </item>
        <item>
            <title>Regulation of cysteine-rich protein 2 localization by the development of actin fibers during smooth muscle cell differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=4998857&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21718689%26dopt%3DAbstract</link>
            <description>Authors: Kihara T, Shinohara S, Fujikawa R, Sugimoto Y, Murata M, Miyake J
    Cysteine-rich protein 2 (CRP2) is a cofactor for smooth muscle cell (SMC) differentiation. Here, we examined the mechanism of CRP2 distribution dynamics during SMC differentiation. CRP2 protein directly associated with F-actin through its N-terminal LIM domain and Gly-rich region, as determined by ELISA. In undifferentiated cells that contain few actin stress fibers, CRP2 was broadly distributed throughout the whole cell, including the nucleus. After induction of SMC differentiation, CRP2 localized to actin stress fibers as they formed. The stress fiber-localized CRP2 entered the nucleus because of induced actin depolymerization. These CRP2 dynamics were reproduced by in silico simulation. CRP2 localization dyna...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998857</comments>
            <pubDate>Sun, 26 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998857</guid>        </item>
        <item>
            <title>Cancer-associated adipocytes promotes breast tumor radioresistance.</title>
            <link>http://www.medworm.com/index.php?rid=4998861&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21712027%26dopt%3DAbstract</link>
            <description>Authors: Bochet L, Meulle A, Imbert S, Salles B, Valet P, Muller C
    Mature adipocytes are excellent candidates to influence tumor behavior through heterotypic signaling processes since these cells produce hormones, growth factors, cytokines and other molecules, a heterogeneous group of molecules named adipokines. Using a 2D coculture system, we demonstrate that breast tumor cells previously co-cultivated with mature adipocytes exhibit radioresistance and an earlier and higher increase in the effector kinase Chk1, a phenotype that was associated with decreased cell death as compared to tumor cells grown alone. Interestingly, the adipocytes-induced tumor changes taking place during the coculture time preceding the exposure to IR were sufficient to confer the radioresistant effect. Notorio...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998861</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998861</guid>        </item>
        <item>
            <title>Perturbations of model membranes induced by pathogenic dynorphin A mutants causing neurodegeneration in human brain.</title>
            <link>http://www.medworm.com/index.php?rid=4998860&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21712028%26dopt%3DAbstract</link>
            <description>Authors: Madani F, Taqi MM, Wärmländer SK, Verbeek DS, Bakalkin G, Gräslund A
    Several effects of the endogenous opioid peptide dynorphin A (Dyn A) are not mediated through the opioid receptors. These effects are generally excitatory, and result in cell loss and induction of chronic pain and paralysis. The mechanism(s) is not well defined but may involve formation of pores in cellular membranes. In the 17-amino acid peptide Dyn A we have recently identified L5S, R6W, and R9C mutations that cause the dominantly inherited neurodegenerative disorder Spinocerebellar ataxia type 23. To gain further insight into non-opioid neurodegenerative mechanism(s), we studied the perturbation effects on lipid bilayers of wild type Dyn A and its mutants in large unilamellar phospholipid vesicles encap...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998860</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998860</guid>        </item>
        <item>
            <title>N-terminal short fragment of TUP1 confers resistance to 5-bromodeoxyuridine in the yeast Saccharomycescerevisiae.</title>
            <link>http://www.medworm.com/index.php?rid=4998859&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21712029%26dopt%3DAbstract</link>
            <description>Authors: Takayama S, Fujii M, Nakagawa Y, Miki K, Ayusawa D
    Small molecules that exhibit biological activity have contributed to the understanding of the molecular mechanisms of various biological phenomena. 5-Bromodeoxyuridine (BrdU) is a thymidine analogue that modulates various biological phenomena such as cellular differentiation and cellular senescence in cultured mammalian cells. Although BrdU is thought to function through changing chromatin structure and gene expression, its precise molecular mechanisms are not understood. To study the molecular mechanism for the action of BrdU, we have employed the yeast Saccharomycescerevisiae as a model system, and screened multi-copy suppressor genes that confer resistance to BrdU. Our genetic screen has revealed that expression of the N-te...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998859</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998859</guid>        </item>
        <item>
            <title>Breast cancer subtypes express distinct receptor repertoires for tumor-associated macrophage derived cytokines.</title>
            <link>http://www.medworm.com/index.php?rid=4998858&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21712030%26dopt%3DAbstract</link>
            <description>Authors: Levano KS, Jung EH, Kenny PA
    Infiltration of the tumor microenvironment by macrophages is associated with poor outcomes in breast cancer and other solid tumors, however the identity and roles of many of the soluble factors these macrophages produce remains to be elucidated in detail. In addition to producing angiogenic factors (e.g. VEGF), proteases (e.g. MMP9) and immunomodulatory factors (e.g. IL10) which, by modifying the local microenvironment, likely contribute to progression in the majority of solid tumors, we have evaluated the extent to which macrophage cytokines may differentially affect distinct breast cancer subtypes. We identified 23 cytokines produced in a culture model of human tumor-associated macrophages and report that basal and luminal breast cancer cell line...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998858</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998858</guid>        </item>
        <item>
            <title>Reduced expression of Tis7/IFRD1 protein in murine and human cystic fibrosis airway epithelial cell models homozygous for the F508del-CFTR mutation.</title>
            <link>http://www.medworm.com/index.php?rid=4998837&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723850%26dopt%3DAbstract</link>
            <description>Authors: Blanchard E, Marie S, Riffault L, Bonora M, Tabary O, Clement A, Jacquot J
    12-O-tetradecanoyl phorbol-13-acetate-induced sequence 7/interferon related development regulator 1 (Tis7/IFRD1) has been recently identified as a modifier gene in lung inflammatory disease severity in patients with cystic fibrosis (CF), based upon its capacity to regulate inflammatory activities in neutrophils. In CF patients, the F508del mutation in the Cftr gene encoding a chloride channel, the CF transmembrane conductance regulator (CFTR) in airway epithelial cells results in an exaggerated inflammatory response of these cells. At present, it is unknown whether the Tis7/IFRD1 gene product is expressed in airway epithelial cells. We therefore investigated the possibility there is an intrinsic alterat...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998837</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998837</guid>        </item>
        <item>
            <title>Enzymatic characterization of Catalase from Bacillus anthracis and prediction of critical residues using information theoretic measure of Relative Entropy.</title>
            <link>http://www.medworm.com/index.php?rid=4998836&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723851%26dopt%3DAbstract</link>
            <description>Authors: Rahi A, Rehan M, Garg R, Tripathi D, Lynn AM, Bhatnagar R
    In order to cope up with the reactive oxygen species (ROS) generated as host innate immune response, most of the intracellular organisms express Catalase for the enzymatic destruction/detoxification of hydrogen peroxide, to combat its deleterious effects. Catalase thus, scavenges ROS thereby playing a pivotal role in facilitating the survival of the pathogen within the host, and thus contributes to its pathogenesis. Bacillus anthracis harbors five isoforms of Catalase, but none of them has been studied so far. Thus, this study is the first attempt to delineate the biochemical and functional characteristics of one of the isoforms of Catalase (Cat1.4) of B. anthracis, followed by identification of residues critical for ca...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998836</comments>
            <pubDate>Thu, 23 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998836</guid>        </item>
        <item>
            <title>Proinsulin maturation disorder is a contributor to the defect of subsequent conversion to insulin in β-cells.</title>
            <link>http://www.medworm.com/index.php?rid=4998853&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723250%26dopt%3DAbstract</link>
            <description>Authors: Wang J, Osei K
    Disproportionate hyperproinsulinemia is an indicator of β-cell dysfunction in diabetes and the basis underlying this abnormality remains obscure. Recently, we have found proinsulin is an aggregation-prone molecule inherent with a low relative folding rate and maintains a homeostatic balance of natively and plentiful non-natively folded states (i.e., proinsulin homeostasis, PIHO) in normal β-cells as a result of the integration of maturation and disposal processes. PIHO is susceptible to environmental and genetic influences. Perturbation of PIHO produces a number of toxic consequences with known association to β-cell failure in diabetes. To explore whether the perturbation of PIHO has a link to disproportionate hyperproinsulinemia, we investigated proinsulin c...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998853</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998853</guid>        </item>
        <item>
            <title>GSK-3β inhibitors suppressed neuroinflammation in rat cortex by activating autophagy in ischemic brain injury.</title>
            <link>http://www.medworm.com/index.php?rid=4998852&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723251%26dopt%3DAbstract</link>
            <description>Authors: Zhou X, Zhou J, Li X, Guo C, Fang T, Chen Z
    Previous studies have shown that GSK-3β inhibitor could reduce infarct volume after ischemia brain injury. However, the underlying mechanisms of GSK-3β inhibitor involving neuroprotection remain poorly understood. In the present study, we demonstrated that GSK-3β inhibitor suppressed insult-induced neuroinflammation in rat cortex by increasing autophagy activation in ischemic injury. Male rats were subjected to pMCAO (permanent middle cerebral artery occlusion) followed by treating with SB216763, a GSK-3β inhibitor. We found that insult-induced inflammatory response was significantly decreased by intraperitoneal infusion of SB216763 in rat cortex. A higher level of autophagy was also detected after SB216763 treatment. In the cult...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998852</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>The pattern of gene expression and gene dose profiles of 6-Mercaptopurine- and 6-Thioguanine-resistant human leukemia cells.</title>
            <link>http://www.medworm.com/index.php?rid=4998851&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723252%26dopt%3DAbstract</link>
            <description>Authors: Karim H, Hashemi J, Larsson C, Moshfegh A, Fotoohi AK, Albertioni F
    Exposure of MOLT4 human T-cell leukemia cells to 6-Mercaptopurine (6-MP) and 6-Thioguanine (6-TG) resulted in acquired resistance associated with attenuated expression of the genes encoding concentrative nucleoside transporter 3 (CNT3) and equilibrative nucleoside transporter 2 (ENT2). To identify other alterations at the RNA and DNA levels associated with 6-MP- and 6-TG resistance, we compared here the patterns of gene expression and DNA copy number profiles of resistant sublines to those of the parental wild-type cells. The mRNA levels for two nucleoside transporters were down-regulated in both of the thiopurine-resistant sublines. Moreover, both of these cell lines expressed genes encoding the enzymes of pu...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998851</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>SERPINB13 is a novel RUNX1 target gene.</title>
            <link>http://www.medworm.com/index.php?rid=4998850&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723253%26dopt%3DAbstract</link>
            <description>Authors: Boyapati A, Ren B, Zhang DE
    RUNX1 is a critical transcription factor during embryogenesis and neoplastic disease. To identify novel transcriptional targets of RUNX1 in the context of chromatin, we performed genome wide location analysis (ChIP-on-chip). Here we report that SERPINB13, a gene downregulated in head and neck cancers, is a novel RUNX1transcriptional target. RUNX1 binds the SERPINB13 promoter in chromatin to repress its transcription. Mutation of either RUNX1 binding site in the SERPINB13 promoter increased the activity of the promoter. Finally, overexpression of RUNX1 and concomitant decrease in SERPINB13 expression led to increased activity of cathepsin K, an enzyme inhibited by SERPINB13. These data demonstrate that RUNX1 is an important regulator of SERPINB13 and...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998850</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Molecular hydrogen inhibits lipopolysaccharide/interferon γ-induced nitric oxide production through modulation of signal transduction in macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=4998849&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723254%26dopt%3DAbstract</link>
            <description>Authors: Itoh T, Hamada N, Terazawa R, Ito M, Ohno K, Ichihara M, Nozawa Y, Ito M
    Molecular hydrogen has been reported to be effective for a variety of disorders and its effects have been ascribed to the reduction of oxidative stress. However, we have recently demonstrated that hydrogen inhibits type I allergy through modulating intracellular signal transduction. In the present study, we examined the hydrogen effects on lipopolysaccharide/interferon γ LPS/IFNγ-induced nitric oxide (NO) production in murine macrophage RAW264 cells. Treatment with hydrogen reduced LPS/IFNγ-induced NO release, which was associated with a diminished induction of inducible isoform of nitric oxide synthase (iNOS). Hydrogen treatment inhibited LPS/IFNγ-induced phosphorylation of apoptosis signal-regulatin...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998849</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Ultrasound-mediated interferon β gene transfection inhibits growth of malignant melanoma.</title>
            <link>http://www.medworm.com/index.php?rid=4998848&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723255%26dopt%3DAbstract</link>
            <description>Authors: Yamaguchi K, Feril LB, Tachibana K, Takahashi A, Matsuo M, Endo H, Harada Y, Nakayama J
    We investigated the effects of ultrasound-mediated transfection (sonotransfection) of interferon β (IFN-β) gene on melanoma (C32) both in vitro and in vivo. C32 cells were sonotransfected with IFN-β in vitro. Subcutaneous C32 tumors in mice were sonicated weekly immediately after intra-tumor injection with IFN-β genes mixed with microbubbles. Successful sonotransfection with IFN-β gene in vitro was confirmed by ELISA, which resulted in C32 growth inhibition. In vivo, the growth ratio of tumors transfected with IFN-β gene was significantly lower than the other experimental groups. These results may lead to a new method of treatment against melanoma and other hard-to-treat cancers.
    ...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998848</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Wisp2/CCN5 up-regulated in the central nervous system of GM3-only mice facilitates neurite formation in Neuro2a cells via integrin-Akt signaling.</title>
            <link>http://www.medworm.com/index.php?rid=4998847&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723256%26dopt%3DAbstract</link>
            <description>In this study, we focused on Wisp2/CCN5 that was up-regulated in nervous tissues in GM3-only mice. Over-expression of Wisp2/CCN5 enhanced neurite outgrowth potently after serum withdrawal with increased phosphorylation levels of Akt and ERKs. When cells were cultured with recombinant Wisp2/CCN5 proteins, more and longer neurites were formed than in the controls. Thus, we demonstrated for the first time that Wisp2/CCN5 facilitates neurite formation in a mouse neuroblastoma cell line, Neuro2a. Akt phosphorylation induced by recombinant Wisp2/CCN5 was suppressed after knockdown of integrin β1. Moreover, Wisp2/CCN5-over-expressing cells were resistant to apoptosis induced by H(2)O(2). These results suggested that secreted Wisp2/CCN5 induces Akt and ERK phosphorylation via integrins, and conse...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998847</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4998847</guid>        </item>
        <item>
            <title>Identification of a putative Crimean-Congo hemorrhagic fever virus entry factor.</title>
            <link>http://www.medworm.com/index.php?rid=4998846&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723257%26dopt%3DAbstract</link>
            <description>Authors: Xiao X, Feng Y, Zhu Z, Dimitrov DS
    Entry of enveloped viruses into cells is initiated by binding of their envelope glycoproteins (Envs) to cell surface-associated receptors. The Crimean-Congo hemorrhagic fever virus (CCHFV) has two Envs, Gn and Gc, with poorly understood role in binding to susceptible cells. We expressed codon optimized Gn and Gc, and identified independently folded soluble Env fragments, one of which (Gc residues 180-300) bound CCHFV susceptible cells supposedly by interacting with a putative receptor. This receptor binding domain (RBD) was used to identify its interacting partner by coimmunoprecipitation and mass spectrometry. Thus we identified the human cell surface nucleolin as a putative CCHFV entry factor. Nucleolin was expressed on all susceptible cell...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998846</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Identification of epigenetically silenced genes in human pancreatic cancer by a novel method &quot;microarray coupled with methyl-CpG targeted transcriptional activation&quot; (MeTA-array).</title>
            <link>http://www.medworm.com/index.php?rid=4998845&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723258%26dopt%3DAbstract</link>
            <description>Identification of epigenetically silenced genes in human pancreatic cancer by a novel method &quot;microarray coupled with methyl-CpG targeted transcriptional activation&quot; (MeTA-array).
    Biochem Biophys Res Commun. 2011 Jun 23;
    Authors: Shimizu H, Horii A, Sunamura M, Motoi F, Egawa S, Unno M, Fukushige S
    Identification and characterization of epigenetically silenced genes is important for cancer research, because information from hypermethylated genes provides clues to understand roles of epigenetics in tumorigeneses and genes frequently methylated in a tumor-specific manner can be used as tumor markers. Here, we describe the identification of transcriptionally silenced hypermethylated genes in pancreatic cancer cells by using a novel method called &quot;microarray coupled with methyl-CpG...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998845</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>The mitochondrial ND1 m.3337G&gt;A mutation associated to multiple mitochondrial DNA deletions in a patient with Wolfram syndrome and cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=4998844&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723259%26dopt%3DAbstract</link>
            <description>We report a Tunisian patient with clinical features of moderate Wolfram syndrome including diabetes, dilated cardiomyopathy and neurological complications. The results showed the presence of the mitochondrial ND1 m.3337G&amp;gt;A mutation in almost homoplasmic form in 3 tested tissues of the proband (blood leukocytes, buccal mucosa and skeletal muscle). In addition, the long-range PCR amplifications revealed the presence of multiple deletions of the mitochondrial DNA extracted from the patient's skeletal muscle removing several tRNA and protein-coding genes. Our study reported a Tunisian patient with clinical features of moderate Wolfram syndrome associated with cardiomyopathy, in whom we detected the ND1 m.3337G&amp;gt;A mutation with mitochondrial multiple deletions.
    PMID: 21723259 [PubMed -...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998844</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Expression of galectin-9 by IFN-γ stimulated human nasal polyp fibroblasts through MAPK, PI3K, and JAK/STAT signaling pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4998843&amp;cid=s_34399_60_f&amp;fid=34399&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21723260%26dopt%3DAbstract</link>
            <description>We examined the correlation between galectin-9 expression and eosinophil infiltration in nasal polyps. In addition, we identified the signaling pathways involved in the elevation of galectin-9 expression in response to IFN-γ. Our data demonstrate that the involvement of mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3 phosphate kinase (PI3K), and Janus kinase/signal transducer and activator of transcription (JAK/STAT) may play important roles in the selective recruitment of eosinophils in nasal polyp tissues through the production of galectin-9. These findings suggest that galectin-9 expression is associated with eosinophil infiltration in polyps of patients with nasal polyposis.
    PMID: 21723260 [PubMed - as supplied by publisher] (Source: Biochemical and Biophysical R...</description>
            <author>Biochemical and Biophysical Research communications</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4998843</comments>
            <pubDate>Wed, 22 Jun 2011 23:00:00 +0100</pubDate>
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