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        <title>Journal of Cellular Biochemistry 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 'Journal of Cellular Biochemistry' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+Cellular+Biochemistry&t=Journal+of+Cellular+Biochemistry&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 13:38:37 +0100</lastBuildDate>
        <item>
            <title>HDAC2 overexpression confers oncogenic potential to human lung cancer cells by deregulating expression of apoptosis and cell cycle proteins</title>
            <link>http://www.medworm.com/index.php?rid=5664010&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24090</link>
            <description>In this study, we demonstrated the aberrant expression of HDAC2 in lung cancer tissues and investigated oncogenic properties of HDAC2 in human lung cancer cell lines. HDAC2 inactivation resulted in regression of tumor cell growth and activation of cellular apoptosis via p53 and Bax activation and Bcl2 suppression. In cell cycle regulation, HDAC2 inactivation caused induction of p21WAF1/CIP1 expression, and simultaneously suppressed the expressions of cyclin E2, cyclin D1 and CDK2, respectively. Consequently, this led to the hypophosphorylation of pRb protein in G1/S transition and thereby inactivated E2F/DP1 target gene transcriptions of A549 cells. In addition, we demonstrated that HDAC2 directly regulated p21WAF1/CIP1 expression in a p53‐independent manner. However, HDAC1 was not rel...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5664010</comments>
            <pubDate>Mon, 06 Feb 2012 18:03:24 +0100</pubDate>
            <guid isPermaLink="false">5664010</guid>        </item>
        <item>
            <title>Decursin inhibits vasculogenesis in early tumor progression by suppression of endothelial progenitor cell differentiation and function</title>
            <link>http://www.medworm.com/index.php?rid=5656171&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24085</link>
            <description>In this study, we investigated whether decursin regulates EPC differentiation and function to inhibit tumor vasculogenesis. We isolated AC133+ cells from human cord blood and decursin significantly decreased the number of EPC colony forming units of human cord blood‐derived AC133+ cells that produce functional EPC progenies. Decursin dose‐dependently decreased the cell number of EPC committing cells as demonstrated by EPC expansion studies. Decursin inhibited EPC differentiation from progenitor cells into spindle‐shaped EPC colonies. Additionally, decursin inhibited proliferation and migration of early EPCs isolated from mouse bone marrow. Furthermore, decursin suppressed expression of angiopoietin‐2, angiopoietin receptor Tie‐2, Flk‐1 (vascular endothelial growth factor recept...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656171</comments>
            <pubDate>Fri, 03 Feb 2012 18:20:18 +0100</pubDate>
            <guid isPermaLink="false">5656171</guid>        </item>
        <item>
            <title>Phenotypic characterization of transgenic mice harboring Nf1+/− or Nf1‐/‐ osteoclasts in otherwise Nf1+/+ background</title>
            <link>http://www.medworm.com/index.php?rid=5664012&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24088</link>
            <description>This study shows that Nf1‐deficiency in osteoclasts may have a role in the development of NF1‐related skeletal abnormalities, but Nf1‐deficiency in osteoclasts in Nf1+/+ background is not sufficient to induce skeletal abnormalities analogous to those observed in patients with neurofibromatosis type 1. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5664012</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5664012</guid>        </item>
        <item>
            <title>The relationships between Snail1 and estrogen receptor signaling in breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5664011&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24087</link>
            <description>ConclusionsIn general, the results obtained demonstrate the phenomenon of Snail1 activation in the hormone‐resistant breast cancer cells, and show that Snail1 and NF‐κB may serve as an important targets in the treatment of breast cancer, both estrogen‐dependent and estrogen‐independent tumors. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5664011</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5664011</guid>        </item>
        <item>
            <title>Phosphorylation target site specificity for AGC kinases DMPK E and Lats2</title>
            <link>http://www.medworm.com/index.php?rid=5656175&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24086</link>
            <description>AbstractSerine/threonine kinases of the AGC group are important regulators of cell growth and motility. To examine the candidate substrate profile for two members of this group, DMPK E and Lats2, we performed in vitro kinase assays on peptide arrays. Substrate peptides for both kinases exhibited a predominance of basic residues surrounding the phosphorylation target site. 3D homology modeling of the kinase domains of DMPK E and Lats2 indicated that presence of two negative pockets in the peptide binding groove provides an explanation for the substrate preference. These findings will aid future research towards signaling functions of Lats2 and DMPK E within cells. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656175</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656175</guid>        </item>
        <item>
            <title>Deep sequencing reveals predominant expression of miR‐21 amongst the small noncoding RNAs in retinal microvascular endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5656174&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24084</link>
            <description>AbstractThe retinal vascular endothelium is essential for angiogenesis and is involved in maintaining barrier selectivity and vascular tone. The aim of this study was to identify and quantify microRNAs and other small regulatory non‐coding RNAs (ncRNAs) which may regulate these crucial functions. Primary bovine retinal microvascular endothelial cells (RMECs) provide a well characterized in vitro system for studying angiogenesis. RNA extracted from RMECs was used to prepare a small RNA library for deep sequencing (Illumina Genome Analyzer). A total of 6.8 million reads were mapped to 250 known microRNAs in miRBase (release 16). In many cases the most frequent isomiR differed from the sequence reported in miRBase. In addition, 6 novel microRNAs, 27 novel bovine orthologs of known human mic...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656174</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656174</guid>        </item>
        <item>
            <title>Clinical significance of circulating interleukin‐23 as a prognostic factor in breast cancer patients</title>
            <link>http://www.medworm.com/index.php?rid=5656173&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24083</link>
            <description>DiscussionThis work investigated, for the first time, the role of IL‐23 in breast cancer patients showing a significant increase respect the control group. However, further validations are needed in larger studies to better investigate the implications of IL‐23 increase in these patients. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656173</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656173</guid>        </item>
        <item>
            <title>Overexpression of hTERT extends replicative capacity of human nucleus pulposus cells, and protects against serum starvation‐induced apoptosis and cell cycle arrest</title>
            <link>http://www.medworm.com/index.php?rid=5656172&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24082</link>
            <description>AbstractThe nucleus pulposus cells are chondrocyte‐like cells that are required for the resistance of compressive loads through the synthesis of collagen fibrils and proteoglycan aggrecans, and the generation of a hydrostatic swelling pressure, and thus play an important role in the intervertebral disc. Here we report the production and characterization of an immortalized human nucleus pulposus (NP) cell line from normal nucleus pulposus cells using stable transfection of recombinant human telomerase reverse transcriptase (hTERT) gene. The hTERT‐transfected nucleus pulposus cells exhibited morphological characteristics typical of native cells. When compared with the first generation of normal nucleus pulposus cells, the hTERT‐transfected nucleus pulposus cells grew faster and had an ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5656172</comments>
            <pubDate>Wed, 01 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5656172</guid>        </item>
        <item>
            <title>Inhibition of IGF‐IR increases chemosensitivity in human colorectal cancer cells through MRP‐2 promoter suppression</title>
            <link>http://www.medworm.com/index.php?rid=5624444&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24080</link>
            <description>AbstractThe emergence of Multidrug resistance (MDR) in cancer cells has made many of the currently available chemotherapeutic agents ineffective. However, the mechanism involved in mediating this effect is not yet fully understood. Here, we found the overexpression of Type I insulin‐like growth factor receptor (IGF‐IR) in established colorectal MDR cells. Specific siRNA of IGF‐IR decreases cell proliferation, exert synergistic effect with anticancer drugs. The downstream signaling of IGF‐IR, PI3K/AKT pathway, was altered upon IGF‐IR silencing. The expression of multidrug‐resistance‐associated protein 2 (MRP‐2) was suppressed due to the nuclear translocation of Nuclear factor‐like 2 (Nrf2). Then the intracellular drug concentration was increased and the drugresistant pheno...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624444</comments>
            <pubDate>Tue, 24 Jan 2012 18:42:43 +0100</pubDate>
            <guid isPermaLink="false">5624444</guid>        </item>
        <item>
            <title>Human umbilical cord Wharton's jelly stem cell (hWJSC) extracts inhibit cancer cell growth in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5624455&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24073</link>
            <description>AbstractUmbilical cord mesenchymal stem cells (MSCs) have been shown to inhibit breast cancer cell growth but it is not known whether this effect is specific to only breast cancer cells. We compared the effects of human Wharton's jelly stem cell (hWJSC) extracts [conditioned medium (hWJSC‐CM) and cell lysate (hWJSC‐CL)] on breast adenocarcinoma (MDA‐MB‐231), ovarian carcinoma (TOV‐112D) and osteosarcoma (MG‐63) cells. The cells were treated with either hWJSC‐CM (50%) or hWJSC‐CL (15μg/ml) for 48 h‐72 h and changes in cell morphology, proliferation, cycle, gene expression, migration and cell death studied. All three cancer cell lines showed cell shrinkage, blebbing and vacuolations with hWJSC‐CL and hWJSC‐CM compared to controls. MTT and BrdU assays showed inhibition ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624455</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624455</guid>        </item>
        <item>
            <title>3‐hydroxy 3‐methylglutaryl coenzyme a reductase inhibition impairs muscle regeneration</title>
            <link>http://www.medworm.com/index.php?rid=5624454&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24077</link>
            <description>AbstractSkeletal muscle has the ability to regenerate new muscle fibers after injury. The process of new muscle formation requires that quiescent mononuclear muscle precursor cells (myoblasts) become activated, proliferate, differentiate, and fuse into multinucleated myotubes which, in turn, undergo further differentiation and mature to form functional muscle fibers. Previous data demonstrated the crucial role played by 3‐hydroxy 3‐methylglutaryl Coenzyme A reductase (HMGR), the rate limiting enzyme of cholesterol biosynthetic pathway, in fetal rat myoblast (L6) differentiation. This finding, along with epidemiological studies assessing the myotoxic effect of statins, HMGR inhibitors, allowed us to speculate that HMGR could be strongly involved in skeletal muscle repair. Thus, our rese...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624454</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624454</guid>        </item>
        <item>
            <title>HMGB1 mediates IFN‐γ‐induced cell proliferation in MMC cells through regulation of cyclin D1/CDK4/p16 pathway</title>
            <link>http://www.medworm.com/index.php?rid=5624452&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24071</link>
            <description>AbstractPrevious studies have revealed the elevated serum levels of High‐mobility group box‐1(HMGB1) and the interferon‐γ (IFN‐γ)‐induced proliferation of renal mesangial cells in patients or experimental animals with systemic lupus erythematosus(SLE). However, it is still not elucidated whether HMGB1 involves in the pathogenesis of lupus nephritis (LN) and mediates IFN‐γ‐induced mesangial cell proliferation. Therefore, in the present study we demonstrated HMGB1 mRNA and protein levels were increased in the glomeruli of LN patients and BXSB mice. HMGB1 increased the proliferation index of mouse mesangial cells (MMC) that was accompanied with the up‐regulation of cyclin D1, CDK4 and the down‐regulation of p16, subsequently promoting the transition from the G0/G1 to S st...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624452</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624452</guid>        </item>
        <item>
            <title>Comparing the biological characteristics of adipose tissue‐derived stem cells of different persons</title>
            <link>http://www.medworm.com/index.php?rid=5624451&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24070</link>
            <description>AbstractScientists have found that cell sex is a variable that considerably influences the regeneration abilities of muscle‐derived stem cells'(MDSCs) in mice.We try to find out whether the cell sex or cell age(the age of donor) will influence the biological characteristics of human adipose tissue‐derived stem cells(H‐ADSCs).The results indicate that cell sex influences the proliferation, differentiation, paracrine and anti‐apoptosis abilities of the H‐ADSCs, and cell age may also affect the H‐ADSCs' differentiation and anti‐apoptosis abilities. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624451</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624451</guid>        </item>
        <item>
            <title>Downregulation of ErbB3 By Wnt3a Contributes to Wnt‐induced osteoblast differentiation in mesenchymal cells</title>
            <link>http://www.medworm.com/index.php?rid=5624450&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24076</link>
            <description>In this study, using microarray analysis we found that Wnt3a upregulates neuregulin 1 (NRG‐1) during Wnt3a‐induced osteoblast differentiation in primary human MSC and murine C3H10T1/2 mesenchymal cells. Western blot and qPCR analyses confirmed that NRG‐1 is up‐regulated by Wnt3a, and that this effect was counterbalanced by decreased expression of the NRG‐1 receptor ErbB3. Consistently, exogenous NRG‐1 had no effect on alkaline phosphatase (ALP) activity, an early marker of osteoblast differentiation. In contrast, small interfering RNA‐mediated silencing of endogenous NRG‐1 increased basal and Wnt3a‐induced ALP activity in MSC. We showed that short hairpin (sh) ErbB3 and Wnt3a additively increased β‐catenin transcriptional activity and ALP activity in MSC. These effects...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624450</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624450</guid>        </item>
        <item>
            <title>MiR‐221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression</title>
            <link>http://www.medworm.com/index.php?rid=5624449&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24075</link>
            <description>In conclusion, our results demonstrated that miR‐221 regulated cardiomyocyte hypertrophy probably through down‐regulation of p27, suggesting that miR‐221 may be a new intervention target for cardiac hypertrophy J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624449</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624449</guid>        </item>
        <item>
            <title>Sphingosine‐1‐ phosphate is a mediator of TNF‐α action on the Na+/K+ ATPase in HepG2 cells</title>
            <link>http://www.medworm.com/index.php?rid=5624448&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24079</link>
            <description>AbstractWe showed previously that TNF‐α down‐regulates the Na+/ K+ ATPase in HepG2 cells. This work was undertaken to study the role of ceramide and its metabolites in TNF‐α action. Treating HepG2 cells with the cytokine in presence of an inhibitor of sphingomyelinase, abrogated the effect of TNF‐α on the ATPase. To confirm the involvement of ceramide or its metabolites, cells were incubated with exogenous ceramide. Ceramide reduced time‐dependently the activity of the ATPase and its effect disappeared in presence of CAY 10466 or SHKI, respective inhibitors of ceramidase and spingosine kinase, suggesting that ceramide acts via sphingosine or sphingosine‐1‐phosphate (S1P). However, HepG2 cells treated with exogenous sphingosine showed a higher Na + /K+ ATPase acti...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624448</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624448</guid>        </item>
        <item>
            <title>Tumor suppressor function of RUNX3 in breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5624447&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24074</link>
            <description>AbstractEmerging evidence indicates that RUNX3 is a tumor suppressor in breast cancer. RUNX3 is frequently inactivated in human breast cancer cell lines and cancer samples by hemizygous deletion of the Runx3 gene, hypermethylation of the Runx3 promoter, or cytoplasmic sequestration of RUNX3 protein. Inactivation of RUNX3 is associated with the initiation and progression of breast cancer. Female Runx3+/− mice spontaneously develop ductal carcinoma, and overexpression of RUNX3 inhibits the proliferation, tumorigenic potential, and invasiveness of breast cancer cells. This review is intended to summarize these findings and discuss the tumor suppressor function of RUNX3 in breast cancer. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624447</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624447</guid>        </item>
        <item>
            <title>Protein kinase Cδ but not PKCα is involved in insulin‐induced glucose metabolism in hepatocytes</title>
            <link>http://www.medworm.com/index.php?rid=5624446&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24078</link>
            <description>In this study we investigated the possibility that these isoforms are involved in the mediation of insulin‐induced glycogen synthesis in hepatocytes. Studies were done on rat hepatocytes in primary culture and on the AML‐12 (Alpha Mouse Liver) cell line. Insulin increased activity and tyrosine phosphorylation of PKCδ within 5 min. In contrast, activity and tyrosine phosphorylation of PKCα were not increased by insulin. PKCδ was constitutively associated with IR, and this was increased by insulin stimulation. Suppression of PKCδ expression by transfection with RNAi, or overexpression of kinase dead (Dominant Negative) PKCδ reduced both the insulin‐induced activation of PKB/Akt and the phosphorylation of Glycogen Synthase Kinase 3 (GSK3) and reduced significantly insulin‐induc...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624446</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624446</guid>        </item>
        <item>
            <title>Microarray‐based identification of aminopeptidase N target genes in keratinocyte conditioned medium‐stimulated dermal fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=5616829&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23438</link>
            <description>AbstractOf the many processes that affect the outcome of wound repair, epidermal–dermal interactions are essential to extracellular matrix (ECM) remodeling and in particular, soluble factors released by keratinocytes are known to have a direct impact on the production of ECM by dermal fibroblasts. Aminopeptidase N (APN) has recently been proposed as a cell‐surface receptor for stratifin and is responsible for the stratifin‐mediated matrix metalloproteinase‐1 (MMP‐1) upregulation in fibroblasts. The present study examines whether modulation of APN gene expression has any impact on the fibroblast ECM gene expression profile. The result reveals that in the presence of keratinocyte‐derived soluble factors, transient knockdown of APN in dermal fibroblasts affects the expression of k...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5616829</comments>
            <pubDate>Sat, 21 Jan 2012 18:16:15 +0100</pubDate>
            <guid isPermaLink="false">5616829</guid>        </item>
        <item>
            <title>Characterization and optimization of a simple, repeatable system for the long term in vitro culture of aligned myotubes in 3D</title>
            <link>http://www.medworm.com/index.php?rid=5616828&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23437</link>
            <description>AbstractIncreased recent research activity in exercise physiology has dramatically improved our understanding of skeletal muscle development and physiology in both health and disease. Advances in bioengineering have enabled the development of biomimetic 3D in vitro models of skeletal muscle which have the potential to further advance our understanding of the fundamental processes that underpin muscle physiology. As the principle structural protein of the extracellular matrix, collagen‐based matrices are popular tools for the creation of such 3D models but the custom nature of many reported systems has precluded their more widespread adoption. Here we present a simple, reproducible iteration of an established 3D in vitro model of skeletal muscle, demonstrating both the high levels of repr...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5616828</comments>
            <pubDate>Sat, 21 Jan 2012 18:16:13 +0100</pubDate>
            <guid isPermaLink="false">5616828</guid>        </item>
        <item>
            <title>In vivo magnetic resonance imaging tracking of SPIO‐labeled human umbilical cord mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5616827&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23432</link>
            <description>In conclusion, hUC‐MSCs can survive and migrate in the host spinal cord after transplantation, which promote functional recovery after SCI. Noninvasive imaging of transplanted SPIO‐labeled hUC‐MSCs is feasible. J. Cell. Biochem. 113: 1005–1012, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5616827</comments>
            <pubDate>Sat, 21 Jan 2012 18:16:07 +0100</pubDate>
            <guid isPermaLink="false">5616827</guid>        </item>
        <item>
            <title>Hydrocortisone attenuates cyclosporin A‐induced nephrotoxicity in rats</title>
            <link>http://www.medworm.com/index.php?rid=5616826&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23429</link>
            <description>This study clearly suggests the role of oxidative stress in the pathogenesis of CsA‐induced nephrotoxicity. J. Cell. Biochem. 113: 997–1004, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5616826</comments>
            <pubDate>Sat, 21 Jan 2012 18:16:06 +0100</pubDate>
            <guid isPermaLink="false">5616826</guid>        </item>
        <item>
            <title>Features: Volume 113, Number 3</title>
            <link>http://www.medworm.com/index.php?rid=5616825&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24268</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5616825</comments>
            <pubDate>Sat, 21 Jan 2012 18:15:29 +0100</pubDate>
            <guid isPermaLink="false">5616825</guid>        </item>
        <item>
            <title>Table of Contents: Volume 113, Number 3</title>
            <link>http://www.medworm.com/index.php?rid=5616824&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24266</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5616824</comments>
            <pubDate>Sat, 21 Jan 2012 18:15:28 +0100</pubDate>
            <guid isPermaLink="false">5616824</guid>        </item>
        <item>
            <title>Journal of Cellular Biochemistry: Volume 113, Number 3, March, 2012</title>
            <link>http://www.medworm.com/index.php?rid=5616823&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24267</link>
            <description>AbstractCover: Morphological organization of NMVMs adherent onto HYALONECT®meshes. See article in this issue by Gallina et al., pages 800–807. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5616823</comments>
            <pubDate>Sat, 21 Jan 2012 18:15:26 +0100</pubDate>
            <guid isPermaLink="false">5616823</guid>        </item>
        <item>
            <title>The cytoprotective effect of butin against oxidative stress is mediated by the up‐regulation of manganese superoxide dismutase expression through a PI3K/Akt/Nrf2‐dependent pathway</title>
            <link>http://www.medworm.com/index.php?rid=5603638&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24068</link>
            <description>The objective of the present study was to elucidate the mechanism by which butin protects mitochondria. The antioxidant function of manganese superoxide dismutase (Mn SOD) is important in preventing oxidative stress. While exposure to H2O2 reduced the expression of Mn SOD in Chinese hamster lung fibroblast (V79‐4), the addition of butin restored Mn SOD expression at both the mRNA and protein levels, resulting in increased Mn SOD activity. The transcription factor NF‐E2‐related factor 2 (Nrf2) regulates Mn SOD gene expression by binding to the antioxidant response element (ARE). Butin enhanced the nuclear translocation and ARE‐binding activity of Nrf2, which was decreased by H2O2. The siRNA‐mediated knockdown of Nrf2 attenuated butin‐induced Mn SOD expression and activity. Furth...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5603638</comments>
            <pubDate>Wed, 18 Jan 2012 19:09:43 +0100</pubDate>
            <guid isPermaLink="false">5603638</guid>        </item>
        <item>
            <title>Cyr61 increases matrix metalloproteinase‐3 expression and cell motility in human oral squamous cell carcinoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5603642&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24066</link>
            <description>In this study, we found that Cyr61 increased the migration and the expression of matrix metalloproteinases‐3 (MMP)‐3 in human OSCC cells. αvβ5 or α6β1 monoclonal antibody (mAb), focal adhesion kinase (FAK) inhibitor, and mitogen‐activated protein kinase (MEK) inhibitors (PD98059 and U0126) inhibited the Cyr61‐induced increase of the migration and MMP‐3 up‐regulation of OSCC cells. Cyr61 stimulation increased the phosphorylation of FAK, MEK, and extracellular signal‐regulated kinase (ERK). In addition, NF‐κB inhibitors suppressed the cell migration and MMP‐3 expression enhanced by Cyr61. Moreover, Cyr61 increased NF‐κB luciferase activity and binding of p65 to the NF‐κB element on the MMP‐3 promoter. Taken together, our results indicate that Cyr61 enhances the...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5603642</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5603642</guid>        </item>
        <item>
            <title>Maintenance of redox state and pancreatic beta‐cell function: Role of leptin and adiponectin</title>
            <link>http://www.medworm.com/index.php?rid=5603641&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24065</link>
            <description>In this study we investigate the importance of maintaining cellular redox state on pancreatic beta‐cell function and viability, and the effects of leptin and adiponectin on this balance. Experiments were conducted on RINm and MIN6 pancreatic beta‐cells. Leptin (1‐100 ng/ml) and adiponectin (1‐100 nM) increased ROS accumulation, as was determined by DCFDA fluorescence. Using specific inhibitors, we found that the increase in ROS levels was mediated by NADPH oxidase, but not by AMPK or PI3K. Leptin and adiponectin increased beta‐cell number as detected by the XTT method, but did not affect apoptosis, indicating that the increased cell number results from increased proliferation. The adipokines‐induced increase in viability is ROS dependent as this effect was abolished by N‐ac...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5603641</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5603641</guid>        </item>
        <item>
            <title>Pro‐apoptotic gene knockdown mediated by nanocomplexed siRNA reduces radiation damage in primary salivary gland cultures</title>
            <link>http://www.medworm.com/index.php?rid=5603640&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24064</link>
            <description>AbstractA critical issue in the management of head and neck tumors is radioprotection of the salivary glands. We have investigated whether siRNA‐mediated gene knock down of pro‐apoptotic mediators can reduce radiation‐induced cellular apoptosis in salivary gland cells in vitro. We used novel, pH‐responsive nanoparticles to deliver functionally active siRNAs into cultures of salivary gland cells. The nanoparticle molecules are comprised of cationic micelles that electrostatically interact with the siRNA, protecting it from nuclease attack, and also include pH‐responsive endosomolytic constituents that promote release of the siRNA into the target cell cytoplasm. Transfection controls with Cy3‐tagged siRNA/nanoparticle complexes showed efficiently internalized siRNAs in more than ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5603640</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5603640</guid>        </item>
        <item>
            <title>Arachidonate 5 lipoxygenase expression in papillary thyroid carcinoma promotes invasion via MMP‐9 induction</title>
            <link>http://www.medworm.com/index.php?rid=5603639&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24069</link>
            <description>AbstractArachidonate 5‐lipoxygenase (ALOX5) expression and activity has been implicated in tumor pathogenesis, yet its role in papillary thyroid carcinoma (PTC) has not been characterized. ALOX5 protein and mRNA were upregulated in PTC compared to matched, normal thyroid tissue, and ALOX5 expression correlated with invasive tumor histopathology. Evidence suggests that PTC invasion is mediated through the induction of matrix metalloproteinases (MMPs) that can degrade and remodel the extracellular matrix (ECM). A correlation between MMP‐9 and ALOX5 protein expression was established by immunohistochemical analysis of PTC and normal thyroid tissues using a tissue array. Transfection of ALOX5 into a PTC cell line (BCPAP) increased MMP‐9 secretion and cell invasion across an ECM barrier. ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5603639</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5603639</guid>        </item>
        <item>
            <title>TGFβ‐inducible early gene‐1 (TIEG1) mutations in hypertrophic cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=5592634&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24058</link>
            <description>AbstractHypertrophic cardiomyopathy (HCM) is the most common heritable cardiovascular disease. A recent study showed that male KLF10‐encoded TGFβ Inducible Early Gene‐1 knock‐out mice (TIEG‐/‐) develop HCM with 13‐fold up‐regulation of PTTG1‐encoded pituitary tumor‐transforming gene 1. We hypothesized TIEG1 could be a novel candidate gene in the pathogenesis of genotype negative HCM in humans, possibly through a loss of its repression on PTTG1 expression. A cohort of 923 unrelated patients from two independent HCM centers was analyzed for mutations in TIEG's 4 translated exons using DHPLC and direct DNA‐sequencing. Site directed mutagenesis was performed to clone novel variants. The effect of TIEG1 mutations on SMAD7 and PTTG1 promoters was studied using transient tran...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592634</comments>
            <pubDate>Sun, 15 Jan 2012 07:29:34 +0100</pubDate>
            <guid isPermaLink="false">5592634</guid>        </item>
        <item>
            <title>Euscaphic acid isolated from roots of Rosa rugosa inhibits LPS‐induced inflammatory responses via TLR4‐mediated NF‐κB inactivation in RAW 264.7 macrophages</title>
            <link>http://www.medworm.com/index.php?rid=5592644&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24062</link>
            <description>AbstractAs an attempt to search for bioactive natural products exerting anti‐inflammatory activity, we have evaluated the anti‐inflammatory effects of euscaphic acid (19α‐hydroxyursane‐type triterpenoids, EA) isolated from roots of Rosa rugosa and its underlying molecular mechanisms in lipopolysaccharide (LPS)‐induced RAW 264.7 macrophages. EA concentration‐dependently reduced the production of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor‐α (TNF‐α), and interleukin‐1β (IL‐1β) induced by LPS in RAW 264.7 macgophages. Consistent with these data, expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase‐2 (COX‐2) protein and iNOS, COX‐2, TNF‐α, and IL‐1β mRNA were inhibited by EA in a concentration‐dependent mann...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592644</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592644</guid>        </item>
        <item>
            <title>Nek2A contributes to tumorigenic growth and possibly functions as potential therapeutic target for human breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5592643&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24059</link>
            <description>ConclusionsThese data suggested that Nek2A might bear a close relationship with development and progression of breast carcinoma, and highlighted its role as a novel potential biomarker for diagnosis and a possible therapeutic target for human breast cancer especially for DCIS. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592643</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592643</guid>        </item>
        <item>
            <title>Inhibition of gecko GSK‐3β promotes elongation of neurites and oligodendrocyte processes but decreases the proliferation of blastemal cells</title>
            <link>http://www.medworm.com/index.php?rid=5592642&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24053</link>
            <description>AbstractGSK‐3β signaling is involved in regulation of both neuronal and glial cell functions, and interference of the signaling affects CNS development and regeneration. Thus, GSK‐3β was proposed to be an important therapeutic target for promoting functional recovery of adult CNS injuries. To further clarify the regulatory function of the kinase on the CNS regeneration, we characterized gecko GSK‐3β and determined the effects of GSK‐3β inactivation on the neuronal and glial cell lines, as well as on the gecko tail (including spinal cord) regeneration. Gecko GSK‐3β shares 91.7%‐96.7% identity with those of other vertebrates, and presented higher expression abundance in brain and spinal cord. The kinase strongly colocalized with the oligodendrocytes while less colocalized wi...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592642</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592642</guid>        </item>
        <item>
            <title>Human umbilical cord Wharton's jelly mesenchymal stem cells do not transform to tumor‐associated fibroblasts in the presence of breast and ovarian cancer cells unlike bone marrow mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5592641&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24057</link>
            <description>AbstractHuman bone marrow mesenchymal stem cells (hBMMSCs) were shown to transform into tumor‐associated fibroblasts (TAFs) when in the vicinity of breast cancer tumors and played an important role in tumor enhancement and metastasis. In early human development MSCs migrating from the yolk sac and aorta‐gonad‐mesonephros (AGM) via the umbilical cord to the placenta and back to the fetal bone marrow were shown to get trapped in the gelatinous Wharton's jelly of the umbilical cord. The common origin of the Wharton's jelly MSCs and the finally homed hBMMSCs prompted us to evaluate whether hWJSCs are also involved in TAF transformation. hWJSCs and hBMMSCs were grown in the presence of breast and ovarian cancer cell conditioned medium (MDA‐TCM, TOV‐TCM) for 30 days. No changes were ob...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592641</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592641</guid>        </item>
        <item>
            <title>Heme induced oxidative stress attenuates sirtuin1 and enhances adipogenesis in mesenchymal stem cells and mouse pre‐adipocytes</title>
            <link>http://www.medworm.com/index.php?rid=5592640&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24061</link>
            <description>AbstractPatho‐physiological conditions with high oxidative stress, such as conditions associated with increased denatured heme‐proteins, are associated with enhanced adipogenic response. This effect predominantly manifests as adipocyte hypertrophy characterized by dysfunctional, pro‐inflammatory adipocytes exhibiting reduced expression of anti‐inflammatory hormone, adiponectin. To understand how increased levels of cellular heme, a pro‐oxidant molecule, modulates adipogenesis; the following study was designed to evaluate effects of heme on adipogenesis in human mesenchymal stem cells (hMSCs) and mouse pre‐adipocytes (3T3L1). Experiments were conducted in the absence and in the presence of a superoxide dismutase mimetic (tempol, 100µM). Heme (10µM) increased (p &amp;lt; 0.05) ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592640</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592640</guid>        </item>
        <item>
            <title>The inhibition of hyaluronan degradation reduced pro‐inflammatory cytokines in mouse synovial fibroblasts subjected to collagen‐induced arthritis</title>
            <link>http://www.medworm.com/index.php?rid=5592639&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24054</link>
            <description>AbstractHyaluronan (HA) degradation produces small oligosaccharides that are able to increase pro‐inflammatory cytokines in rheumatoid arthritis synovial fibroblasts (RASF) by activating both CD44 and the toll‐like receptor 4 (TLR‐4). CD44 and TLR‐4 stimulation in turn activate the NF‐kB that induces the production of pro‐inflammatory cytokines. Degradation of HA occurs via two mechanisms: one exerted by reactive oxygen species (ROS) and one controlled by different enzymes in particular hyaluronidases (HYALs). We aimed to investigate the effects of inhibiting HA degradation (which prevents the formation of small HA fragments) on synovial fibroblasts obtained from normal DBA/J1 mice (NSF) and on synovial fibroblasts (RASF) obtained from mice subjected to collagen induced arthrit...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592639</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592639</guid>        </item>
        <item>
            <title>Three‐dimensional epithelial and mesenchymal cell co‐cultures form early tooth epithelium invagination‐like structures: Expression patterns of relevant molecules</title>
            <link>http://www.medworm.com/index.php?rid=5592638&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24056</link>
            <description>In this study, we built a three dimensional model to represent epithelium invagination‐like structure by tissue engineering. Human normal oral epithelial cells (OECs) and dental pulp stem cells (DPSCs) were co‐cultivated for 2‐7 weeks on matrigel or collagen gel to form epithelial and mesenchymal tissues. The histological change and gene expression were analyzed by HE staining, immunostaining and quantitative real time RT‐PCR (qRT‐PCR). After 4 weeks of cultivation, OECs‐formed epithelium invaginated into DPSCs‐derived mesenchyme on both matrigel and collagen gel. OEC‐DPSC co‐cultures on matrigel showed typical invagination of epithelial cells and condensation of the underlying mesenchymal cells. Epithelial invagination related molecules, CD44 and E‐cadherin, and mesenc...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592638</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592638</guid>        </item>
        <item>
            <title>Overexpression of the long non‐coding RNA MEG3 impairs in vitro glioma cell proliferation</title>
            <link>http://www.medworm.com/index.php?rid=5592637&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24055</link>
            <description>AbstractGliomas are the most common type of primary brain tumor in the central nervous system of adults. Maternally Expressed Gene 3 (MEG3) is an imprinted gene located at 14q32 that encodes a non‐coding RNA associated with tumorigenesis. However, little is known about whether and how MEG3 regulates glioma development. In the present study we assayed the expression of MEG3 in glioma tissue samples by real‐time polymerase chain reaction assay, and defined the biological functions and target genes by CCK‐8 assay, flow cytometry and RNA immunoprecipitation. We firstly demonstrated that MEG3 expression was markedly decreased in glioma tissues compared with adjacent normal tissues. Moreover, ectopic expression of MEG3 inhibited cell proliferation and promoted cell apoptosis in U251 and U8...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592637</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592637</guid>        </item>
        <item>
            <title>The PPARδ ligand L‐165041 inhibits VEGF‐induced angiogenesis, but the antiangiogenic effect is not related to PPARδ</title>
            <link>http://www.medworm.com/index.php?rid=5592636&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24063</link>
            <description>This study highlights the therapeutic potential of L‐165041 in the treatment of many disorders related to pathological angiogenesis. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592636</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592636</guid>        </item>
        <item>
            <title>Effects of medium calcium, and agents affecting cytoskeletal function, on cellular volume and morphology in liver tissue in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5592635&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24060</link>
            <description>In conclusion, our results are consistent with the hypothesis that iso‐osmotic expulsion of water from hepatocytes can proceed partly through an accumulation of water in cytoplasmic vesicles, followed by exocytosis. This mechanism does not depend on Na+‐ K+ ATPase activity. J. Cell. Biochem. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5592635</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5592635</guid>        </item>
        <item>
            <title>Development, characterization, and applications of a novel estrogen receptor beta monoclonal antibody</title>
            <link>http://www.medworm.com/index.php?rid=5568510&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23443</link>
            <description>AbstractThe role of estrogen receptor alpha (ERα) in breast cancer has been studied extensively, and its protein expression is prognostic and a primary determinant of endocrine sensitivity. However, much less is known about the role of ERβ and its relevance remains unclear due to the publication of conflicting reports. Here, we provide evidence that much of this controversy may be explained by variability in antibody sensitivity and specificity and describe the development, characterization, and potential applications of a novel monoclonal antibody targeting full‐length human ERβ and its splice variant forms. Specifically, we demonstrate that a number of commercially available ERβ antibodies are insensitive for ERβ and exhibit significant cross‐reaction with ERα. However, our new...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568510</comments>
            <pubDate>Sat, 07 Jan 2012 00:41:27 +0100</pubDate>
            <guid isPermaLink="false">5568510</guid>        </item>
        <item>
            <title>Pro‐inflammatory cytokines induce odontogenic differentiation of dental pulp‐derived stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5568509&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23396</link>
            <description>In this study, the effects of pro‐inflammatory cytokines, such as IL‐1 and TNF, on DPSCs were investigated. Cells were treated with IL‐1, TNF, or both for 3, 7, and 12 days. The cultures were evaluated for cell proliferation, ALP activity, and real‐time PCR. We found that a short treatment (3 days) of pro‐inflammatory cytokines induced the odontogenic differentiation of DPSCs. Furthermore, post 3 days treatment with pro‐inflammatory cytokines, the cell–scaffold complexes were implanted subcutaneously in mice for 8 weeks. Histological analysis demonstrated that the cultures gave obviously mineralized tissue formation, especially for both IL‐1 and TNF applied. These data suggest that IL‐1 and TNF produced in the early inflammatory reaction may induce the mineralization of D...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568509</comments>
            <pubDate>Sat, 07 Jan 2012 00:41:22 +0100</pubDate>
            <guid isPermaLink="false">5568509</guid>        </item>
        <item>
            <title>Atorvastatin suppresses inflammatory response induced by oxLDL through inhibition of ERK phosphorylation, IκBα degradation, and COX‐2 expression in murine macrophages</title>
            <link>http://www.medworm.com/index.php?rid=5568508&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23388</link>
            <description>AbstractMacrophages crosstalk with oxidized low‐density lipoprotein (oxLDL), play a critical role in the initiation, progression, and subsequently stability of atherosclerotic plaques. Statins, inhibitors of HMG CoA (3‐hydroxy‐3‐methylglutaryl coenzyme A) reductase, reduce the expression of inflammatory proteins in addition to their lipid‐lowering action. However, the effect and detailed anti‐inflammation mechanisms of statins in macrophages induced by oxLDL remain unclearly. In the present study, we investigated the effect of atorvastatin on inflammatory response upon oxLDL stimulation in murine macrophages and analyzed the underlying mechanisms. Tumor necrosis factor (TNF)α and monocyte chemoattractant protein‐1 (MCP‐1) mRNA levels were assayed by real‐time PCR. The ex...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568508</comments>
            <pubDate>Sat, 07 Jan 2012 00:41:14 +0100</pubDate>
            <guid isPermaLink="false">5568508</guid>        </item>
        <item>
            <title>Stress‐specific responses of p21 expression: Implication of transcript variant p21 alt‐a in long‐term hypoxia</title>
            <link>http://www.medworm.com/index.php?rid=5568507&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23377</link>
            <description>In this study, we analyzed the effects of various antemortem conditions on p21 protein level and expression profiles of known p21 transcript variants in human heart tissue. The selected death cause groups were: non‐cardiac, hypothermia, acute ischemia, and chronic hypoxia. Immunohistochemical staining of p21 in cardiac myocytes could be observed only in hypothermia death cases, in which the mRNA expression of the most abundant variant, p21V1, also exceeded that in other death cause groups. Cytoplasmic localization of p21 protein in vascular smooth muscle cells together with substantially increased expression of cardioprotective Pim‐1 especially in chronic hypoxia, but in acute ischemia and hypothermia as well, indicate change of p21 function from cell cycle arrest to promotion of proli...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568507</comments>
            <pubDate>Sat, 07 Jan 2012 00:41:04 +0100</pubDate>
            <guid isPermaLink="false">5568507</guid>        </item>
        <item>
            <title>Enhancement of cell–cell contact by claudin‐4 in renal epithelial madin‐darby canine kidney cells</title>
            <link>http://www.medworm.com/index.php?rid=5568506&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23373</link>
            <description>AbstractClaudin‐4 regulates ion permeability via a paracellular pathway in renal epithelial cells, but its other physiological functions have not been examined. We found that hyperosmotic stress increases claudin‐4 expression in Madin‐Darby canine kidney cells. Here, we examined whether claudin‐4 affects cell motility, cell association, and the intracellular distribution of endogenous junctional proteins. Doxycycline‐inducible expression of claudin‐4 did not change endogenous levels of claudin‐1, claudin‐2, claudin‐3, occludin, E‐cadherin, and ZO‐1. Claudin‐4 overexpression increased cell association and decreased cell migration without affecting cell proliferation. Doxycycline did not change cell junctional protein levels, cell association or cell migration in mock...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568506</comments>
            <pubDate>Sat, 07 Jan 2012 00:40:59 +0100</pubDate>
            <guid isPermaLink="false">5568506</guid>        </item>
        <item>
            <title>Manipulation of cellular redox parameters for improving therapeutic responses in B‐cell lymphoma and multiple myeloma</title>
            <link>http://www.medworm.com/index.php?rid=5568505&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23387</link>
            <description>AbstractDeveloping novel combined‐modality therapeutic approaches based on understanding of the involvement of redox biology in apoptosis of malignant cells is a promising approach for improving clinical responses in B‐cell lymphoma and multiple myeloma. Therapeutic modalities that generate reactive oxygen species (i.e., radiation, photodynamic therapy, and specific chemotherapeutic drugs) have been shown to be selectively cytotoxic to malignant B‐cells. In this review, we will discuss agents that induce apoptosis in B‐cell tumors by oxidative stress. Subsequently, a novel biochemical rationale (based on fundamental differences in cancer vs. normal cell oxidative metabolism) for combining oxidative stressors with radiotherapy and chemotherapy, that may lead to designing of more eff...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568505</comments>
            <pubDate>Sat, 07 Jan 2012 00:40:46 +0100</pubDate>
            <guid isPermaLink="false">5568505</guid>        </item>
        <item>
            <title>LTBPs, more than just an escort service</title>
            <link>http://www.medworm.com/index.php?rid=5568504&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23385</link>
            <description>AbstractLatent transforming growth factor beta (TGF‐β) binding proteins (LTBPs) are large extracellular glycoproteins structurally similar to fibrillins. They perform intricate and important roles in the extracellular matrix (ECM) and perturbations of their function manifest as a wide range of diseases. LTBPs are major regulators of TGF‐β bioavailability and action. In addition, LTBPs interact with other ECM proteins—from cytokines to large multi‐factorial aggregates like microfibrils and elastic fibers, affecting their genesis, structure, and performance. In the present article, we review recent advancements in the field and relate the complex roles of LTBP in development and homeostasis. J. Cell. Biochem. 113: 410–418, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568504</comments>
            <pubDate>Sat, 07 Jan 2012 00:40:45 +0100</pubDate>
            <guid isPermaLink="false">5568504</guid>        </item>
        <item>
            <title>Emergence of chondrogenic progenitor stem cells in transplantation biology—prospects and drawbacks</title>
            <link>http://www.medworm.com/index.php?rid=5568503&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23367</link>
            <description>AbstractAvascular tissues such as a cartilage contains a unique type of cell called as the chondrocyte. We, however, have not understood the origin of the chondrocyte population and how this population is maintained in the normal tissue. In spite of being considered to be a simple tissue, scientist had always faced difficulties to engineer this tissue. This is because different structural regions of the articular cartilage were never understood. In addition to this, the limited self‐repair potential of cartilage tissue and lack of effective therapeutic options for the treatment of damaged cartilage has remained an unsolved problem. Mesenchymal stem cell based therapy may provide a solution for cartilage regeneration. This is due to their ability to differentiate into chondrogenic lineage...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568503</comments>
            <pubDate>Sat, 07 Jan 2012 00:40:42 +0100</pubDate>
            <guid isPermaLink="false">5568503</guid>        </item>
        <item>
            <title>Features: Volume 113, Number 2</title>
            <link>http://www.medworm.com/index.php?rid=5568502&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24365</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568502</comments>
            <pubDate>Sat, 07 Jan 2012 00:40:37 +0100</pubDate>
            <guid isPermaLink="false">5568502</guid>        </item>
        <item>
            <title>Table of Contents: Volume 113, Number 2</title>
            <link>http://www.medworm.com/index.php?rid=5568501&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24363</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568501</comments>
            <pubDate>Sat, 07 Jan 2012 00:40:35 +0100</pubDate>
            <guid isPermaLink="false">5568501</guid>        </item>
        <item>
            <title>Journal of Cellular Biochemistry: Volume 113, Number 2, February, 2012</title>
            <link>http://www.medworm.com/index.php?rid=5568500&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24364</link>
            <description>AbstractCover: The cover shows cultured dual‐colored MMT cells with RFP expression in the cytoplasm, and GFP linked to histone H2B, expressed in the nuclei. See article in this issue by Amoh et al, pages 465–472. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568500</comments>
            <pubDate>Sat, 07 Jan 2012 00:40:34 +0100</pubDate>
            <guid isPermaLink="false">5568500</guid>        </item>
        <item>
            <title>Salicylideneamino‐2‐thiophenol enhances osteogenic differentiation through the activation of MAPK pathways in multipotent bone marrow stem cell</title>
            <link>http://www.medworm.com/index.php?rid=5568483&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24052</link>
            <description>In this study, we investigated the effects of Sal‐2 on osteogenic differentiation of multipotent bone marrow stromal stem cells by alizarin red S staining for osteogenic differentiation, RT‐PCR and western blot for alkaline phosphatase (ALP) activity and signaling pathways, FACS analysis and immunofluorescence staining for CD44 and CD51 expression, calcium assays, and immunofluorescence staining for signaling pathways. We found that Sal‐2 enhanced the osteogenic differentiation of multipotent bone marrow stromal stem cells. Sal‐2 treatment induced the expression and activity of ALP, and enhanced the levels of CD44 and CD51 expression as well as Ca2+ content, in multipotent bone marrow stromal stem cells. Moreover, we found that Sal‐2‐induced osteogenic differentiation and expre...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568483</comments>
            <pubDate>Sat, 07 Jan 2012 00:37:56 +0100</pubDate>
            <guid isPermaLink="false">5568483</guid>        </item>
        <item>
            <title>Activation of PKR/eIF2α signaling cascade is associated with dihydrotestosterone‐induced cell cycle arrest and apoptosis in human liver cells</title>
            <link>http://www.medworm.com/index.php?rid=5568485&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24051</link>
            <description>In this study, we investigated the effect of DHT on human liver cells. We found that DHT not only induces cell cycle arrest but also initiates apoptosis in androgen‐sensitive liver cells, such as SMMC‐7721 and L02. Importantly, DHT/AR induces the activation of RNA‐dependent protein kinase (PKR)/eukaryotic initiation factor‐2 (eIF2α) cascades in androgen‐sensitive liver cells. PKR/eIF2α activation‐induced growth arrest and DNA damage‐inducible gene 153 (GADD153) and heat shock protein 27 (Hsp27) expression contribute to cell cycle arrest in response to DHT. It is notable that DHT administration results in androgen‐sensitive liver cells apoptosis, at least in part, through PKR/eIF2α/GADD153 cascades. These results suggest that the androgen/AR pathway plays a pivotal role i...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568485</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568485</guid>        </item>
        <item>
            <title>Medical therapies with adult stem/progenitor cells (MSCs): A backward journey from dramatic results in vivo to the cellular and molecular explanations</title>
            <link>http://www.medworm.com/index.php?rid=5556642&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24046</link>
            <description>AbstractThere is currently great interest in the use of mesenchymal stem/stromal cells (MSCs) for the therapy of many diseases of animals and humans. However, we are still left with the serious challenges in explaining the beneficial effects of the cells. Hence, it is essential to work backward from dramatic results obtained in vivo to the cellular and molecular explanations in order to discover the secrets of MSCs. This review will focus on recent data that have changed the paradigms for understanding the therapeutic potentials of MSCs. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556642</comments>
            <pubDate>Sun, 01 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5556642</guid>        </item>
        <item>
            <title>Effects of indoxyl sulfate on adherens junctions of endothelial cells and the underlying signaling mechanism</title>
            <link>http://www.medworm.com/index.php?rid=5549450&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23435</link>
            <description>This study explored the effects of IS on the adherens junctions of vascular endothelial cells and revealed the underlying mechanism. Bovine pulmonary artery endothelial cells (BPAECs) were treated with IS, and the distribution of vascular endothelial cadherin (VE‐cadherin), p120‐catenin, β‐catenin, and stress fibers was examined by immunofluorescence. IS treatment resulted in disruption of intercellular contacts between BPAECs with prominent parallel‐oriented intracellular stress fiber formation. Intracellular free radical levels which measured by flow cytometry increased after IS treatment. The antioxidant, MnTMPyP, and an ERK pathway inhibitor, U0126, both significantly prevented IS‐induced disruption of intercellular contacts. Western blotting analyses demonstrated that IS in...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549450</comments>
            <pubDate>Thu, 29 Dec 2011 10:48:10 +0100</pubDate>
            <guid isPermaLink="false">5549450</guid>        </item>
        <item>
            <title>Phosphorylation of serine 21 modulates the proliferation inhibitory more than the differentiation inducing effects of C/EBPα in K562 cells</title>
            <link>http://www.medworm.com/index.php?rid=5549462&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24040</link>
            <description>AbstractThe CCAAT/Enhancer binding protein α (C/EBPα) is a transcription factor required for differentiation of myeloid progenitors. In acute myeloid leukemia (AML) cells expressing the constitutively active FLT3‐ITD receptor tyrosine kinase, MAP kinase‐dependent phosphorylation of serine 21 (S21) inhibits the ability of C/EBPα to induce granulocytic differentiation To assess whether this post‐translational modification also modulates the activity of C/EBPα in BCR/ABL‐expressing cells, we tested the biological effects of wild type and mutant C/EBPα mimicking phosphorylated or non–phosphorylatable serine 21 (S21D and S21A, respectively) in K562 cells ectopically expressing tamoxifen‐regulated C/EBPα‐ER chimeric proteins.We show here that S21D C/EBPα‐ER induced termi...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549462</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549462</guid>        </item>
        <item>
            <title>Non‐coding RNAs as theranostics in human cancers</title>
            <link>http://www.medworm.com/index.php?rid=5549461&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24038</link>
            <description>AbstractTheranostics was coined originally as a term used to describe a system that combines diagnosis and therapy, aiming to provide the tools for personalized medicine. This review reasserts the grounds for regarding non‐coding RNAs as theranostics in human cancers. MiRNAs are the most well studied non‐coding RNAs in recent years; their pivotal role in orchestrating tumor initiation and progression has been confirmed in all types of cancers. Hence, these small non‐coding RNAs have emerged as attractive therapeutic targets and diagnostic tool. Various approaches to use their therapeutic potential have been taken, here we summarize the most important ones. In the near future, the focus of theranostics will be shifted towards longer and mechanistically more versatile ncRNAs, and we in...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549461</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549461</guid>        </item>
        <item>
            <title>Chemical transfection of dye‐conjugated microRNA precursors for microRNA functional analysis of M2 macrophages</title>
            <link>http://www.medworm.com/index.php?rid=5549460&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24041</link>
            <description>ConclusionsAmong the most common methods of transfection, the chemical transfection of dye‐conjugated miRNA precursors was determined to be the best suited approach for the functional analysis of M2 macrophages. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549460</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549460</guid>        </item>
        <item>
            <title>Phosphofructokinase type 1 kinetics, isoform expression and gene polymorphisms in cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5549459&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24039</link>
            <description>AbstractKinetic analysis of PFK‐1 from rodent AS‐30D, and human HeLa and MCF‐7 carcinomas revealed sigmoidal [Fru6P]‐rate curves with different Vm values when varying the allosteric activator Fru2,6BP, AMP, Pi, NH or K+. The rate equation that accurately predicted this behavior was the exclusive ligand binding concerted transition model together with non‐essential hyperbolic activation. PFK‐1 from rat liver and heart also exhibited the mixed cooperative‐hyperbolic kinetic behavior regarding activators. Lowering pH induced decreased affinity for Fru6P, Fru2,6BP, citrate, and ATP (as inhibitor); as well as decreased Vm and increased content of inactive (T) enzyme forms. High K+ prompted increased (Fru6P) or decreased (activators) affinities; increased Vm; and increased content ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549459</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549459</guid>        </item>
        <item>
            <title>A2a adenosine receptor mediates HepG2 cell apoptosis by downregulating Bcl‐XL expression and upregulating bid expression</title>
            <link>http://www.medworm.com/index.php?rid=5549458&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24048</link>
            <description>AbstractExtracellular adenosine induced apoptosis in HepG2 cells, a human hepatoma cell line, by tuning apoptosis‐mediator gene transcription. The present study aimed at identifying the responsible adenosine receptor and clarifying the signaling pathway underlying adenosine‐induced HepG2 cell apoptosis. Adenosine and CGS21680, an A2a adenosine receptor agonist, induced HepG2 cell apoptosis, and the effect was inhibited by DMPX, an A2a adenosine receptor antagonist, or by knocking‐down A2a adenosine receptors. Adenosine reduced expression of Bcl‐XL mRNA and protein but otherwise increased expression of the Bid mRNA and protein in HepG2 cells, and those effects were also prevented by knocking‐down A2a adenosine receptors. Adenosine caused disruption of mitochondrial membrane potent...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549458</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549458</guid>        </item>
        <item>
            <title>Odontogenic ameloblasts‐associated protein (ODAM), via phosphorylation by bone morphogenetic protein receptor type IB (BMPR–IB), is implicated in ameloblast differentiation</title>
            <link>http://www.medworm.com/index.php?rid=5549457&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24047</link>
            <description>AbstractTo elucidate the function of the odontogenic ameloblast‐associated protein (ODAM) in ameloblasts, we identified more than 74 proteins that interact with ODAM using protoarray. Of the identified proteins, bone morphogenetic protein receptor type‐IB (BMPR‐IB) was physiologically relevant in differentiating ameloblasts. ODAM and BMPR‐IB exhibited similar patterns of expression in vitro, during ameloblast differentiation. ODAM and BMPR‐IB interacted through the C‐terminus of ODAM, which resulted in increased ODAM phosphorylation in the presence of bone morphogenetic protein 2 (BMP‐2). Immunoprecipitation assays using Ser‐Xaa‐Glu (SXE) mutants of ODAM demonstrated that the phosphorylation of ODAM by BMPR‐IB occurs at this motif, and this phosphorylation is required f...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549457</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549457</guid>        </item>
        <item>
            <title>Proteomic identification of PSF and p54(nrb) as TopBP1‐interacting proteins</title>
            <link>http://www.medworm.com/index.php?rid=5549456&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24045</link>
            <description>AbstractTopBP1 is a BRCT domain‐rich protein that is structurally and functionally conserved throughout eukaryotic organisms. It is required for the initiation of DNA replication and for DNA repair and damage signalling. To further dissect its biological functions, we explored TopBP1‐interacting proteins by co‐immunoprecipitation assays and LC‐ESI‐MS‐analyses. As TopBP1 binding partners we identified p54(nrb) and PSF, and confirmed the physical interactions by GST pull‐down assays, co‐immunoprecipitations and by yeast two‐hybrid experiments. Recent evidence shows an involvement of p54(nrb) and PSF in DNA double‐strand break repair (DSB) and radioresistance. To get a first picture of the physiological significance of the interaction of TopBP1 with p54(nrb) and PSF we inv...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549456</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549456</guid>        </item>
        <item>
            <title>Characterization of female germ cells derived from mouse embryonic stem cells through expression of GFP under the control of Figla promoter</title>
            <link>http://www.medworm.com/index.php?rid=5549455&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24044</link>
            <description>AbstractPrevious studies have demonstrated that germ cells can be derived from mouse embryonic stem cells (ESCs). However, there is still no efficient system, which can visualize the stage of germ cell specification in vitro, and further to identify and enrich germ cells derived from ESCs. Figla (factor in the germline, alpha) gene encodes a germ cell specific transcription factor that coordinates the expression of the oocyte‐specific zona pellucida (Zp) genes and is essential for folliculogenesis in mouse. Here, we first constructed a pFigla‐EGFP recombinant plasmid that expressed enhanced green fluorescent protein (EGFP) under the control of Figla promoter, and generated and characterized an ESC line stably carrying this pFigla‐EGFP reporter construct. Then the ESCs were induced to...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549455</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549455</guid>        </item>
        <item>
            <title>Silibinin suppresses the maintenance of colorectal cancer stem‐like cells by inhibiting PP2A/AKT/mTOR pathways</title>
            <link>http://www.medworm.com/index.php?rid=5549454&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24043</link>
            <description>This study aimed to examine whether silibinin inhibited the development of CSLCs and disclose the underlying signaling. The colorectal cancer spheroid culture system was used for enriching CSLCs. The effects of silibinin on CSLCs were evaluated by counting sphere numbers, and calculating the percentage of CD133+ cells by flow cytometry and immunofluorescence both in the absence and presence of different concentrations of silibinin. The results showed the sphere number of CCS was 36 ± 9.6 after 15 days of CSLC enrichment in spheroid culture, and the percentage of CD133+ cells increased to 18 ± 6.4% compared to 3 ± 0.8% before enrichment. Treatment with silibinin reduced the sphere formation to 5 ± 3.3 and decreased the CD133+ percentage to 8 ± 2.3%. Interestingly, t...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549454</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549454</guid>        </item>
        <item>
            <title>Streptococcus mutans GS‐5 antigen I/II stimulates cell survival in serum deprived‐cultures through PI3K/Akt pathways</title>
            <link>http://www.medworm.com/index.php?rid=5549453&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24042</link>
            <description>In this study, we examined the effects of the His‐tagged recombinant N‐terminal half of the AgI/II protein (rAgI/II‐N) generated from S. mutans GS‐5 on the viability, proliferation, and cell cycle progression of primary calvarial osteoblasts. We also investigated the mechanisms involved in the rAgI/II‐N‐mediated survival of serum‐starved osteoblasts. We found that rAgI/II treatment attenuated the serum deprivation‐induced decrease in cell viability and proliferation of osteoblasts. rAgI/II‐N also prevented the loss of mitochondrial membrane potential, alterations in levels of two key mitochondrial Bcl‐2 family proteins, and the accumulation of numerous cells into the sub‐G1 phase that were observed in serum‐starved osteoblasts. Pharmacological inhibitors of phosphoi...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549453</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549453</guid>        </item>
        <item>
            <title>Promyelocytic leukemia nuclear bodies support a late step in DNA double‐strand break repair by homologous recombination</title>
            <link>http://www.medworm.com/index.php?rid=5549452&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24050</link>
            <description>We examined the involvement of PML protein and PML‐NB in homologous recombinational repair (HRR) of chromosomal DNA double‐strand breaks. Transient overexpression of wild‐type PML protein isoforms produced hugely enlarged or aggregated PML‐NB and reduced HRR by ∼2 fold, suggesting that HRR depends to some extent upon normal PML‐NB structure. Knockdown of PML by RNA interference sharply attenuated formation of PML‐NB and reduced HRR by up to 20 fold. However, PML‐knockdown cells showed apparently normal induction of H2AX phosphorylation and RAD51 foci after DNA damage by ionizing radiation. These findings indicate that early steps in HRR, including recognition of DNA double‐strand breaks, initial processing of ends, and assembly of single‐stranded DNA/RAD51 nucleoprotein...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549452</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549452</guid>        </item>
        <item>
            <title>Lanthanum chloride bidirectionally influences calcification in bovine vascular muscle smooth cells</title>
            <link>http://www.medworm.com/index.php?rid=5549451&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24049</link>
            <description>In this study, we used bovine vascular smooth muscle cells as a model vascular calcification in vitro and studied the effects of lanthanum chloride on calcium deposition. Exposure of cells to LaCl3 at the concentration of 0.1 µ M suppressed the β‐glycerophosphate‐induced alkaline phosphatase activity and calcium deposition. Furthermore, LaCl3 upregulated the β‐glycerophosphate‐suppressed expression of calcium‐sensing receptor. In contrast to the inhibitory effect of LaCl3 on calcium deposition, higher level lanthanum (50µ M) was found to promote immediately precipitation of calcium phosphate in cell culture medium. At this concentration, LaCl3 was found induced cell apoptosis which involves caspase‐9 and ‐3. These data indicate that the promotory effect of LaCl3 on calciu...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549451</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5549451</guid>        </item>
        <item>
            <title>Features: Volume 113, Number 1</title>
            <link>http://www.medworm.com/index.php?rid=5532949&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24262</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532949</comments>
            <pubDate>Fri, 23 Dec 2011 07:21:05 +0100</pubDate>
            <guid isPermaLink="false">5532949</guid>        </item>
        <item>
            <title>Table of Contents: Volume 113, Number 1</title>
            <link>http://www.medworm.com/index.php?rid=5532948&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24260</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532948</comments>
            <pubDate>Fri, 23 Dec 2011 07:21:03 +0100</pubDate>
            <guid isPermaLink="false">5532948</guid>        </item>
        <item>
            <title>Journal of Cellular Biochemistry: Volume 113, Number 1, January, 2012</title>
            <link>http://www.medworm.com/index.php?rid=5532947&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24261</link>
            <description>AbstractCover: The cover shows rapamycin inhibition of Epo‐dependent osteoblast differentiation in hBMSC cells. See article in this issue by Kim et al, pages 220–228. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532947</comments>
            <pubDate>Fri, 23 Dec 2011 07:21:02 +0100</pubDate>
            <guid isPermaLink="false">5532947</guid>        </item>
        <item>
            <title>The cyclin‐dependent kinase inhibitor roscovitine inhibits kinase activity, cell proliferation, multicellular development, and Cdk5 nuclear translocation in Dictyostelium discoideum</title>
            <link>http://www.medworm.com/index.php?rid=5532923&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23417</link>
            <description>AbstractRoscovitine, a cyclin‐dependent kinase (Cdk) inhibitor, inhibited kinase activity and the axenic growth of Dictyostelium discoideum at micromolar concentrations. Growth was almost fully rescued in 50 µM and ∼50% rescued in 100 µM roscovitine‐treated cultures by the over‐expression of Cdk5‐GFP. This supports the importance of Cdk5 function during cell proliferation in Dictyostelium and indicates that Cdk5 is a primary target of the drug. Roscovitine did not affect the expression of Cdk5 protein during axenic growth but did inhibit its nuclear translocation. This novel result suggests that the effects of roscovitine could be due in part to altering Cdk5 translocation in other systems as well. Kinase activity was inhibited by roscovitine in assays using AX3 whole cell ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532923</comments>
            <pubDate>Fri, 23 Dec 2011 07:18:05 +0100</pubDate>
            <guid isPermaLink="false">5532923</guid>        </item>
        <item>
            <title>Oxidative‐mechanical stress signals stem cell niche mediated Lrp5 osteogenesis in eNOS‐/‐ null mice</title>
            <link>http://www.medworm.com/index.php?rid=5532931&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24031</link>
            <description>ConclusionTargeting the Wnt3a/Lrp5 pathway in valve calcification and activation of osteogenesis is via an oxidative‐mechanical stress in CAVD. These findings provide a foundation for treating this disease process by targeting the cross talk mechanism in a resident stem cell niche. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532931</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532931</guid>        </item>
        <item>
            <title>Endothelial cell surface expression of protein disulfide isomerase activates β1 and β3 integrins and facilitates dengue virus infection</title>
            <link>http://www.medworm.com/index.php?rid=5532930&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24037</link>
            <description>AbstractInfection with dengue virus (DENV) causes diseases ranging from mild dengue fever to severe hemorrhage or shock syndrome. DENV infection of endothelial cells may cause cell apoptosis or vascular leakage and result in clinical illness of hemorrhage. However, the endothelial cell molecules involved in DENV infection and the mechanisms governing virus‐cell interactions are still uncertain. Since protein diisulfide isomerase (PDI) reducing function at the cell surface was shown to be required for entry of certain viruses and bacteria, we explored the role of PDI expressed on endothelial cell surface in DENV infection. Using siRNA to knock down PDI, DENV infection was reduced which could be reversed by treating cells with a reducing agent Tris(2‐carboxyethyl)phosphine hydrochloride ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532930</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532930</guid>        </item>
        <item>
            <title>Calcineurin serves in the circadian output pathway to regulate the daily rhythm of L‐type voltage‐gated calcium channels in the retina</title>
            <link>http://www.medworm.com/index.php?rid=5532929&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23419</link>
            <description>In this study, we report that calcineurin, a Ca2+/calmodulin‐dependent serine (ser)/threonine (thr) phosphatase, participates in the circadian output pathway to regulate L‐VGCCs through modulating both Ras‐MAPK and Ras‐PI3K‐AKT signaling. The activity of calcineurin, but not its protein expression, was under circadian regulation. Application of a calcineurin inhibitor, FK‐506 or cyclosporine A, reduced the L‐VGCC current density at night with a corresponding decrease in L‐VGCCα1D protein expression, but the circadian rhythm of L‐VGCCα1D mRNA levels were not affected. Inhibition of calcineurin further reduced the phosphorylation of ERK and AKT (at thr 308) and inhibited the activation of Ras, but inhibitors of MAPK or PI3K signaling did not affect the circadian rhythm of...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532929</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532929</guid>        </item>
        <item>
            <title>miRNA expression profile during osteogenic differentiation of human adipose‐derived stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5532927&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23418</link>
            <description>ConclusionsWe identified a group of miRNAs that may play important roles in regulating hADSC cell differentiation toward an osteoblast lineage. Further study of these miRNAs may elucidate the mechanism of hADSC differentiation into adipose tissue, and thus provide basis for tissue engineering. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532927</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532927</guid>        </item>
        <item>
            <title>The hinge region of the scaffolding protein of cell contacts, zonula occludens protein 1, regulates interacting with various signaling proteins</title>
            <link>http://www.medworm.com/index.php?rid=5532926&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23422</link>
            <description>In conclusion, proteins with different regulatory potential adhere to and influence cellular functions of ZO‐proteins, and the interactions can be modulated via its hinge region and/or the binding proteins. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532926</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532926</guid>        </item>
        <item>
            <title>Zinc balance is critical for NFI‐C mediated regulation of Odontoblast differentiation</title>
            <link>http://www.medworm.com/index.php?rid=5532925&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23421</link>
            <description>AbstractZinc is trace element essential for diverse metabolic and cellular signaling pathways for the growth, development, and maintenance. Zinc deficiency is involved in bone malformations and oral disease. Mice deficient in zinc transporter Zip13 show connective tissue and skeletal disorders, abnormal incisor teeth, and reduced root dentin formation in the molar teeth and share a morphologically similar phenotype to nuclear factor I‐C (NFI‐C)‐deficient mice. However, the precise function of zinc in NFI‐C signaling‐mediated odontoblast differentiation and dentin formation remains unclear. Here, we show that zinc stimulated the expression of metal transcription factor‐1, but decreased NFI‐C expression in odontoblastic MDPC‐23 cells. Zinc also enhanced the phosphorylation ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532925</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532925</guid>        </item>
        <item>
            <title>Restraint of spreading‐dependent activation of polymorphonuclear leukocyte NADPH oxidase in an acidified environment</title>
            <link>http://www.medworm.com/index.php?rid=5532924&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23416</link>
            <description>AbstractElucidation of the mechanisms by which environmental pH affects or regulates the functions of polymorphonuclear leukocytes (PMNs) is important because severe acidification of the microenvironment often prevails at sites of inflammation where they act in host defense. In the present study, we investigated the effect of an acidic environment on spreading‐dependent activation of O‐producing NADPH oxidase in PMNs. We found that PMNs underwent spreading spontaneously over type I collagen and plastic surfaces at both neutral and acidic pH, although spreading over fibrinogen surfaces, for which cellular stimulation with H2O2 is required, was inhibited by acidic pH. At acidic pH, however, PMNs were unable to undergo spreading‐dependent production of O. Pharmacological experiments sho...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532924</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532924</guid>        </item>
        <item>
            <title>Thapsigargin down‐regulates protein levels of GRP78/BiP in INS‐1E cells</title>
            <link>http://www.medworm.com/index.php?rid=5532936&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24032</link>
            <description>AbstractPancreatic β‐cells have a well developed endoplasmic reticulum (ER) and express large amounts of chaperones and protein disulfide isomerases (PDI) to meet the high demand for synthesis of proteins. We have observed an unexpected decrease in chaperone protein level in the β‐cell model INS1‐E after exposure to the ER stress inducing agent thapsigargin. As these cells are a commonly used model for primary β‐cells and has been shown to be vulnerable to ER stress, we hypothesize these cells are incapable of mounting a chaperone defense upon activation of ER stress. To investigate the chaperone expression during an ER stress response, induced by thapsigargin in INS‐1E cells, we used quantitative mass spectrometry based proteomics.The results displayed a decrease of GRP78/BiP...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532936</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532936</guid>        </item>
        <item>
            <title>Proteomic investigation of 5‐fluorouracil resistance in a human hepatocellular carcinoma cell line</title>
            <link>http://www.medworm.com/index.php?rid=5532935&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24036</link>
            <description>AbstractMultidrug resistance (MDR) is a major obstacle towards a successful treatment of hepatocellular carcinoma (HCC). The mechanisms of MDR are intricate and have not been fully understood. Therefore, we employed a cell‐line model consisting of the 5‐fluorouracil (5‐FU) resistant BEL7402/5‐FU cell line and its parental BEL7402 cell line. Using iTRAQ‐coupled 2D LC‐MS/MS, a successfully exploited high‐throughput proteomic technology, in total, 660 unique proteins were identified and 52 proteins showed to be differentially expressed in BEL7402/5‐FU compared with BEL7402. Several differentially expressed proteins were further validated by Western blot and real‐time quantitative RT‐PCR analysis. Furthermore, the association of MDR with ANXA3, one of the highly expressed p...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532935</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532935</guid>        </item>
        <item>
            <title>The hydroxylation activity of Jmjd6 is required for its homo‐oligomerization</title>
            <link>http://www.medworm.com/index.php?rid=5532934&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24035</link>
            <description>In this study, we examined the enzymatic activity of Jmjd6 and uncovered the mechanism underlying its homo‐oligomerization. An in vitro enzymatic assay monitored by matrix‐assisted laser desorption‐ionization time‐of‐flight (MALDI‐TOF) mass spectrometry indicates that Jmjd6 is unable to remove the methyl group from histone arginine residues but can hydroxylate the histone H4 tail at lysine residues in a 2‐oxoglutarate (2‐OG)‐ and Fe (II)‐dependent manner. A mutational analysis reveals that the homo‐oligomerization of Jmjd6 requires its enzymatic activity and the N‐ and C‐termini. Using an in vitro enzymatic assay, we further demonstrate that Jmjd6 can hydroxylate its N‐terminus but not its C‐terminus. In summary, we did not detect arginine demethylase activity...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532934</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532934</guid>        </item>
        <item>
            <title>Umami taste receptor functions as an amino acid sensor via Gαs subunit in N1E‐115 neuroblastoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5532933&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24034</link>
            <description>AbstractThe sensing of the nutritional level of the body fluid is pivotal for maintaining homeostasis in animals. However, it is not yet understood how the cells detect nutritional levels. In the present study, we examined the function of umami taste receptor, which has a dimeric protein structure composed of Tas1r1 and Tas1r3, as amino acid sensor in the cells. We found that deprivation of amino acids induced neurite outgrowth in N1E‐115 cells. The neurite outgrowth was inhibited by almost all of the amino acids tested. To investigate the involvement of the umami taste receptor, siRNA against each of Tas1r1 or Tas1r3 was administered, resulting in suppression of the inhibitory effects of amino acids on neurite outgrowth. In addition, inosine 5'‐monophosphate, which potentiates the r...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532933</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532933</guid>        </item>
        <item>
            <title>Characterization of hydrophobic anti‐cancer drug‐loaded amphiphilic peptides as a gene carrier</title>
            <link>http://www.medworm.com/index.php?rid=5532932&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24033</link>
            <description>AbstractAn amphiphilic peptide with a 3‐arginine stretch and a 6‐valine stretch was evaluated as a gene carrier. The short amphiphilic peptide, R3V6, not only formed micelles in aqueous solution, butwas also able to deliver plasmid DNA (pDNA) into cells without toxicity. In this research, various amphiphilic peptides were synthesized with a 3‐arginine stretch and a 6‐valine, ‐alanine, ‐leucine, or ‐phenylalanine stretch.In vitro transfection assays in human embryonic kidney 293 cells showed that R3V6 and R3L6 peptides had higher transfection efficiencies than R3A6, R3F6 and poly‐L‐lysine (PLL). Since the peptide micelles had hydrophobic cores, a hydrophobic anti‐cancer drug, bis‐chloronitrosourea (BCNU),was able to be loaded into the cores of the micelles. The incor...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5532932</comments>
            <pubDate>Tue, 20 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5532932</guid>        </item>
        <item>
            <title>Macrophage migration inhibitory factor increases cell motility and up‐regulates αvβ3 integrin in human chondrosarcoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5512044&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24027</link>
            <description>AbstractThe macrophage migration‐inhibitory factor (MIF) is a pro‐inflammatory cytokine first known for its effect on macrophage migration and activation. Recent studies have shown that MIP plays a critical role in tumor growth, angiogenesis, and metastasis. Chondrosarcoma is a type of highly malignant tumor with a potent capacity to invade locally and cause distant metastasis. However, the effects of MIF on human chondrosarcoma cells are largely unknown. In the present study, MIF was found to increase the migration and the expression of αvβ3 integrin in human chondrosarcoma cells. The phosphatidylinositol 3‐kinase (PI3K), Akt, and NF‐κB pathways were activated by MIF treatment, and the MIF‐induced expression of integrin and migration activity were inhibited by the specific in...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512044</comments>
            <pubDate>Sat, 17 Dec 2011 06:49:57 +0100</pubDate>
            <guid isPermaLink="false">5512044</guid>        </item>
        <item>
            <title>Small molecule induction of neural‐like cells from bone marrow‐mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5512059&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24021</link>
            <description>We report here that LY294002, a small molecule inhibitor of PI3K/AKT signal pathway, can inhibit proliferation and promote neuronal differentiation of MSCs after MSCs incubated with LY294002 for 6h and 12h. RT‐PCR results indicated that mRNA expression ofα5β1 integrin significantly increased in neuron‐like cell from MSCs. Interestingly, neuron‐like cells derived by this method adhere much more strongly than MSCs, which was related to the expression of α5β1 integrin and FAK phosphorylation. However, these effects could be attenuated by LiCL or GSK‐3β ‐siRNA. Our results indicate that activation GSK‐3β signaling may be involved in MSCs proliferation, differentiation and adhesion. Furthermore, this study demonstrates that small molecule regulators of PI3K/AKT signalling may ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512059</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512059</guid>        </item>
        <item>
            <title>PA28β regulates cell invasion of gastric cancer via modulating the expression of chloride intracellular channel 1</title>
            <link>http://www.medworm.com/index.php?rid=5512058&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24022</link>
            <description>AbstractPA28β is a subunit of proteasome activator PA28. Previous study suggests that PA28β is involved in the invasiveness and metastasis of gastric adenocarcinoma (GA), however, the mechanism is not fully understood. In the present study, we showed that invasive abilities of gastric cancer cells were enhanced when PA28β being down‐regulated, and were inhibited when PA28β being over expressed. To explore the possible mechanism of PA28β associated elevated invasiveness, the protein profiles of PA28β knock down and parental negative control gastric cancer cells were compared using proteomics approach. The results revealed that there were 43 proteins were differentially expressed, among them, chloride intracellular channel 1 (CLIC1) was significantly up‐regulated and selected for f...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512058</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512058</guid>        </item>
        <item>
            <title>CaM Kinase control of AKT and LNCaP cell survival</title>
            <link>http://www.medworm.com/index.php?rid=5512057&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24020</link>
            <description>AbstractAKT and its substrate BAD have been shown to promote prostate cancer cell survival. Agonists, such as carbachol, and hormones that increase intracellular calcium concentration can activate AKT leading to cancer cell survival. The LNCaP prostate cancer cells express the carbachol‐sensitive M3‐subtype of GPCR's that cause increases in intracellular calcium and activate the family of Ca2+/Calmodulin‐dependent Protein Kinases (CaM Ks). One type of CaM Kinase, CaM Kinase Kinase (CaM KK), phosphorylates several substrates including AKT on threonine 308. AKT phosphorylation and activation enhances cell survival through phosphorylation of BAD protein and the subsequent blockade of caspase activation. Our goals were to examine the mechanism of carbachol activation of AKT and BAD in LN...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512057</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512057</guid>        </item>
        <item>
            <title>Activation of Notch‐1 enhances epithelial‐mesenchymal transition in gefitinib‐acquired resistant lung cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5512056&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24019</link>
            <description>AbstractDespite an initial response to EGFR tyrosine kinase inhibitors (EGFR TKI) in EGFR mutant lung cancer, most patients eventually become resistant and result in treatment failure. Recent studies have shown that epithelial to mesenchymal transition (EMT) is associated with drug resistance and cancer cell metastasis. Strong multiple gene signature data indicate that EMT acts as a determinant of insensitivity to EGFR TKI. However, the exact mechanism for the acquisition of the EMT phenotype in EGFR‐TKI resistant lung cancer cells remains unclear. In the present study, we showed that the expression of Notch‐1 was highly upregulated in gefitinib‐resistant PC9/AB2 lung cancer cells. Moreover, the Notch‐1 receptor intracellular domain (N1IC), the activated form of the Notch‐1 recep...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512056</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512056</guid>        </item>
        <item>
            <title>Upregulation of mTORC2 activation by the selective agonist of EPAC, 8‐CPT‐2Me‐cAMP, in prostate cancer cells: Assembly of a multi‐protein signaling complex</title>
            <link>http://www.medworm.com/index.php?rid=5512055&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24018</link>
            <description>AbstractLigation of cell surface‐associated GRP78 by activated α2‐macroglobulin triggers pro‐proliferative cellular responses. In part, this results from activation of adenylyl cyclase leading to an increse in cAMP. We have previously employed the cAMP analogue 8‐CPT‐2Me‐cAMP to probe these responses. Here we show in 1‐LN prostate cancer cells that 8‐CPT‐2Me‐cAMP causes a dose‐dependent increase in Epac1, p‐AktT308, p‐AktS473, but not p‐CREB. By contrast, the PKA activator 6‐Benz‐cAMP caused a dose‐dependent increase in p‐CREB, but not Epac1. We measured mTORC2‐dependent Akt phosphorylation at S473 in immunoprecipitates of mTOR or Rictor from 1‐LN cells. 8‐CPT‐2Me‐cAMP caused a two‐threefold increase in p‐AktS473 and AktS473 kinase activit...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512055</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512055</guid>        </item>
        <item>
            <title>Continuously generated H2O2 stimulates the proliferation and osteoblastic differentiation of human periodontal ligament fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=5512054&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24017</link>
            <description>In this study, we examined how H2O2 affects the viability and proliferation of PLF by exposing the cells to glucose oxidase (GO) or direct addition of H2O2. We also explored the effects of GO on the osteoblastic differentiation of PLF and the mechanisms involved. The viability and proliferation in PLF were increased with the addition of 10 mU/ml GO but not by volumes greater than 15 mU/ml or by H2O2 itself. GO‐stimulated DNA synthesis was correlated with the increase in cyclin E protein levels in the cells. Osteoblastic differentiation of PLF was also augmented by combined treatment with GO, as evidenced by the increases in alkaline phosphatase activity, mineralization, collagen synthesis, and osteocalcin content in the cells. The inductions of runt‐related transcription factor 2 and o...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512054</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512054</guid>        </item>
        <item>
            <title>Oxidative stress due to aluminium exposure induces eryptosis which is prevented by erythropoietin</title>
            <link>http://www.medworm.com/index.php?rid=5512053&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24026</link>
            <description>In conclusion, results provide evidence that chronic Al exposure may lead to biochemical and morphological alterations similar to those shown in eryptosis induced by oxidant compounds in human erythrocytes. The antieryptotic effect of EPO may contribute to enhance the knowledge of its physiological role on erythroid cells. Irrespective of the antioxidant mechanism, this property of EPO, shown in this model of Al exposure, let us suggest potential benefits by EPO treatment of patients with anaemia associated to altered redox environment. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512053</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512053</guid>        </item>
        <item>
            <title>Acquisition of MDR phenotype by leukemic cells is associated with increased caspase‐3 activity and a collateral sensitivity to cold stress</title>
            <link>http://www.medworm.com/index.php?rid=5512052&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24016</link>
            <description>AbstractThe acquisition of a multidrug‐resistant (MDR) phenotype by tumor cells that renders them unsusceptible to anti‐neoplasic agents is one of the main causes of chemotherapy failure in human malignancies. The increased expression of P‐glycoprotein (MDR1, P‐gp, ABCB1) in tumor cells contributes to drug resistance by extruding chemotherapeutic agents or by regulating programmed cell death. In a study of MDR cell survival under cold stress conditions, it was found that resistant leukemic cells with P‐gp over‐expression, but not their sensitive counterparts, are hypersensitive to cold‐induced cell death when exposed to temperatures below 4 °C. The transfection of parental cells with a P‐gp‐expressing plasmid makes these cells sensitive to cold stress, demonstrating an a...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512052</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512052</guid>        </item>
        <item>
            <title>IL‐4 induces proliferation in prostate cancer PC3 cells under nutrient‐depletion stress through the activation of the JNK‐pathway and survivin upregulation</title>
            <link>http://www.medworm.com/index.php?rid=5512051&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24025</link>
            <description>AbstractInterleukin (IL)‐4 plays a critical role in the regulation of immune responses and has been detected at high levels in the tumor microenvironment of cancer patients where it correlates with the grade of malignancy. The direct effect of IL‐4 on cancer cells has been associated with increased cell survival; however, its role in cancer cell proliferation and related mechanisms is still unclear. Here it was shown that in a nutrient‐depleted environment, IL‐4 induces proliferation in prostate cancer PC3 cells. In these cells, under nutrient‐depletion stress, IL‐4 activates mitogen‐activated protein kinases (MAPKs), including Erk, p38 and JNK. Using MAP‐signaling‐specific inhibitors, it was shown that IL‐4‐induced proliferation is mediated by JNK activation. In fa...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512051</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512051</guid>        </item>
        <item>
            <title>Molecular mechanisms of early growth response protein‐1 (EGR‐1) expression by quercetin in INS‐1 beta‐cells</title>
            <link>http://www.medworm.com/index.php?rid=5512050&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24024</link>
            <description>AbstractEarly growth response‐1 (EGR‐1), one of immediate early response genes, is involved in diverse cellular response. We recently reported that quercetin increased catalytic subunit of γ‐glutamylcysteine ligase (GCLC) via the interaction of EGR‐1 to GCLC promoter in INS‐1 beta‐cells. Therefore, this study investigated molecular mechanisms of quercetin‐induced EGR‐1 expression in INS‐1 cells. Quercetin significantly induced EGR‐1 protein and its mRNA expressions. This induction of EGR‐1 was completely blocked by pretreatment with a PKA inhibitor, H89 and partially blocked by a p38 inhibitor, SB203580. Additionally, the siRNA‐mediated inhibition of PKAα and p38 resulted in significant reduction of quercetin‐induced EGR‐1 promoter activity. Also, quercetin...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512050</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512050</guid>        </item>
        <item>
            <title>Hyperthermia‐enhanced TRAIL‐ and mapatumumab‐induced apoptotic death is mediated through mitochondria in human colon cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5512049&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24023</link>
            <description>In this study, we evaluated the anti‐tumor efficacy of humanized anti‐death receptor 4 (DR4) antibody mapatumumab (Mapa) by comparing it with TRAIL in combination with hyperthermia. TRAIL, which binds to both DR4 and death receptor 5 (DR5), was approximately 10‐fold more effective than Mapa in inducing apoptosis. However, hyperthermia enhances apoptosis induced by either agent. We observed that the synergistic effect was mediated through elevation of reactive oxygen species, c‐Jun N‐terminal kinase activation, Bax oligomerization and translocalization to the mitochondria, loss of mitochondrial membrane potential, release of cytochrome c to cytosol, activation of caspases and increase in poly(ADP‐ribose) polymerase cleavage. We believe that the successful outcome of this study w...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512049</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512049</guid>        </item>
        <item>
            <title>Chemokine receptor CXCR7 mediates human endothelial progenitor cells survival, angiogenesis, but not proliferation</title>
            <link>http://www.medworm.com/index.php?rid=5512048&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24015</link>
            <description>AbstractStromal cell‐derived factor 1 (SDF‐1) is a critical regulator of endothelial progenitor cells (EPCs) mediated physiological and pathologic angiogenesis. It was considered to act via its unique receptor CXCR4 for a long time. CXCR7 is a second, recently identified receptor for SDF‐1, and its role in human EPCs is unclear. In present study, CXCR7 was found to be scarcely expressed on the surface of human EPCs derived from cord blood, but considerable intracellular CXCR7 was detected, which differs from that on EPCs derived from rat bone marrow. CXCR7 failed to support SDF‐1 induced human EPCs migration, proliferation or nitric oxide (NO) production, but mediated human EPCs survival exclusively. Besides that, CXCR7 mediated EPCs tube formation and matrix metalloproteinase‐2 ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512048</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512048</guid>        </item>
        <item>
            <title>Evaluation of physiological importance of metallothionein protein expressed by Tetrahymena cadmium metallothionein 1 (TMCd1) gene in Escherichia coli</title>
            <link>http://www.medworm.com/index.php?rid=5512047&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24030</link>
            <description>AbstractTMCd1 is a cadmium inducible metallothionein gene. In the present study the TMCd1 gene of a ciliate protozoan has been expressed in E.coli and the function of the expressed TMCd1 protein as a metal binding protein has been evaluated. The growth of E.coli cells expressing the GST fused TMCd1 proteins in the presence of cadmium metal clearly demonstrated the role of TMCd1 as a metal binding protein. The metal accumulation experiments showed that the bacterial cells expressing the functional TMCd1 protein accumulated 19 ‐fold more cadmium in contrast to control cells that lacked the TMCd1 protein expression. The results clearly demonstrate a physiological role of full length TMCd1 protein of a ciliate, expressed in E. coli, in cadmium metal sequestration and detoxification. J. Cell....</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512047</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512047</guid>        </item>
        <item>
            <title>SNX10 is required for osteoclast formation and resorption activity</title>
            <link>http://www.medworm.com/index.php?rid=5512046&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24029</link>
            <description>In this report we describe the expression and functional characterization of Sorting Nexin 10 (snx10). Snx10 belongs to the sorting nexin (SNX) family, a diverse group of proteins with a common feature: the PX domain, which is involved in membrane trafficking and cargo sorting in endosomes. Snx10 is strongly up‐regulated during RANKL‐induced osteoclast differentiation in vitro and expressed in osteoclasts in vivo. qPCR analysis confirmed a significant increase in the expression of snx10 in in vitro‐derived osteoclasts, as well as in femur and calvaria. Immunohistochemical analysis of mouse embryo sections showed expression in long bone, calvariae, and developing teeth. The expression was limited to cells that also expressed TRAP, demonstrating osteoclastic localization. Confocal immu...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512046</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512046</guid>        </item>
        <item>
            <title>Effect of phorbol 12‐myristate 13‐acetate activated signaling pathways on 1α, 25 dihydroxyvitamin D3 regulated human 25‐hydroxyvitamin D3 24‐hydroxylase gene expression in differentiated Caco‐2 cells</title>
            <link>http://www.medworm.com/index.php?rid=5512045&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24028</link>
            <description>AbstractPhorbol‐12‐myristate‐13‐acetate (PMA), a protein kinase C (PKC) activator, can modulate 1α, 25 dihydroxyvitamin D3 (1,25(OH)2D3)‐induced expression of the 24‐hydroxylase (CYP24A1) gene but this has not been studied in differentiated enterocytes, a primary 1,25(OH)2D3 target cell. We found that in differentiated Caco‐2 cells, an established model of the mature absorptive epithelial cell, PMA significantly enhanced 1,25(OH)2D3‐induced human CYP24A1 (hCYP24A1) mRNA accumulation and hCYP24A1 promoter‐luciferase reporter gene activation by 150%. Reporter gene studies further identified the region between ‐298 to +74 bp in the hCYP24A1 promoter as critical for the PMA enhancing effect and chromatin immunoprecipitation (ChIP) analysis showed that PMA enhanced 1,25(O...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5512045</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5512045</guid>        </item>
        <item>
            <title>p38 MAPK activation, JNK inhibition, neoplastic growth inhibition, and increased gap junction communication in human lung carcinoma and Ras‐transformed cells by 4‐Phenyl‐3‐butenoic acid</title>
            <link>http://www.medworm.com/index.php?rid=5492373&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23353</link>
            <description>AbstractHuman lung neoplasms frequently express mutations that down‐regulate expression of various tumor suppressor molecules, including mitogen‐activated protein kinases such as p38 MAPK. Conversely, activation of p38 MAPK in tumor cells results in cancer cell cycle inhibition or apoptosis initiated by chemotherapeutic agents such as retinoids or cisplatin, and is therefore an attractive approach for experimental anti‐tumor therapies. We now report that 4‐phenyl‐3‐butenoic acid (PBA), an experimental compound that reverses the transformed phenotype at non‐cytotoxic concentrations, activates p38 MAPK in tumorigenic cells at concentrations and treatment times that correlate with decreased cell growth and increased cell‐cell communication. H2009 human lung carcinoma cells and...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492373</comments>
            <pubDate>Sun, 11 Dec 2011 07:52:01 +0100</pubDate>
            <guid isPermaLink="false">5492373</guid>        </item>
        <item>
            <title>Experimental hyperprolinemia induces mild oxidative stress, metabolic changes, and tissue adaptation in rat liver</title>
            <link>http://www.medworm.com/index.php?rid=5492372&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23342</link>
            <description>AbstractThe present study investigated the effects of chronic hyperprolinemia on oxidative and metabolic status in liver and serum of rats. Wistar rats received daily subcutaneous injections of proline from their 6th to 28th day of life. Twelve hours after the last injection the rats were sacrificed and liver and serum were collected. Results showed that hyperprolinemia induced a significant reduction in total antioxidant potential and thiobarbituric acid‐reactive substances. The activities of the antioxidant enzymes catalase and superoxide dismutase were significantly increased after chronic proline administration, while glutathione (GSH) peroxidase activity, dichlorofluorescin oxidation, GSH, sulfhydryl, and carbonyl content remained unaltered. Histological analyses of the liver reveal...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492372</comments>
            <pubDate>Sun, 11 Dec 2011 07:51:50 +0100</pubDate>
            <guid isPermaLink="false">5492372</guid>        </item>
        <item>
            <title>Broader utilization of origins of DNA replication in cancer cell lines along a 78 kb region of human chromosome 2q34</title>
            <link>http://www.medworm.com/index.php?rid=5492371&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23336</link>
            <description>In this study, we have employed a real‐time PCR‐based nascent strand DNA abundance assay, to determine the location of origins along a 78 kb region on Chr2q34. Preliminary studies using nascent DNA strands isolated from either HeLa and normal skin fibroblast cells showed that in both cell lines peaks of high origin activity mapped in similar locations. However, the overall origin profile in HeLa cells corresponded to broad origin activation zones, whereas in fibroblasts a more punctuated profile of origin activation was observed. To investigate the relevance of this differential origin profile, we compared the origin distribution profiles in breast cancer cell lines MDA‐MB‐231, BT‐474, and MCF‐7, to their normal counterpart MCF‐10A. In addition, the CRL7250 cell line was al...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492371</comments>
            <pubDate>Sun, 11 Dec 2011 07:51:44 +0100</pubDate>
            <guid isPermaLink="false">5492371</guid>        </item>
        <item>
            <title>Inhibition of Wnt signaling by cucurbitacin B in breast cancer cells: Reduction of Wnt‐associated proteins and reduced translocation of galectin‐3‐mediated β‐catenin to the nucleus</title>
            <link>http://www.medworm.com/index.php?rid=5492370&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23326</link>
            <description>AbstractThe cucurbitacins are tetracyclic triterpenes found in plants of the family Cucurbitaceae. Cucurbitacins have been shown to have anti‐cancer and anti‐inflamatory activities. We investigated the anti‐cancer activity of cucurbitacin B extracted from Thai medicinal plant Trichosanthes cucumerina Linn. Cell viability was assessed by MTT (3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide) assay. Results indicated that cucurbitacin B from T. cucumerina Linn. has a cytotoxic effect on breast cancer cell lines SKBR‐3 and MCF‐7 with an IC50 of 4.60 and 88.75 µg/ml, respectively. Growth inhibition was attributed to G2/M phase arrest and apoptosis. Cyclin D1, c‐Myc, and β‐catenin expression levels were reduced. Western blot analysis showed increased PA...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5492370</comments>
            <pubDate>Sun, 11 Dec 2011 07:51:34 +0100</pubDate>
            <guid isPermaLink="false">5492370</guid>        </item>
        <item>
            <title>Chemical reduction of carboxyl groups in heparin abolishes its vasodilatory activity</title>
            <link>http://www.medworm.com/index.php?rid=5464909&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24008</link>
            <description>AbstractPrevious studies have shown that heparin induces vascular relaxation via integrin‐dependent nitric oxide‐mediated activation of the muscarinic receptor. The aim of this study was to identify the structural features of heparin that are necessary for the induction of vasodilatation. To address this issue, we tested heparin from various sources for their vasodilatation activities in the rat aorta ring. Structural and chemical characteristics of heparin, such as its molecular weight and substitution pattern, did not show a direct correlation with the vasodilation activity. Principal component analysis of circular dichroism, 1H‐nuclear magnetic resonance and vasodilation activity measurements confirmed that there is no direct relationship between the physico‐chemical nature and ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464909</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464909</guid>        </item>
        <item>
            <title>MMP‐3 provokes CTGF/CCN2 production independently of protease activity and dependently on dynamin‐related endocytosis, which contributes to human dental pulp cell migration</title>
            <link>http://www.medworm.com/index.php?rid=5464908&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24007</link>
            <description>In this study, we examined the involvement of CTGF/CCN2 in MMP‐3‐induced cell migration in human dental pulp (fibroblast‐like) cells. In human dental pulp cells, MMP‐3 promoted cell migration, but this effect was clearly blocked in the presence of anti‐CTGF/CCN2 antibody. MMP‐3 provoked mRNA and protein expression and secretion of CTGF/CCN2 in a concentration‐ and time‐dependent manner. The MMP‐3 inhibitor NNGH failed to suppress MMP‐3‐induced CTGF/CCN2 protein expression. The potent dynamin inhibitor dynasore clearly inhibited MMP‐3‐induced CTGF/CCN2 expression. These results strongly suggest that MMP‐3 induces CTGF/CCN2 production independently of the protease activity of MMP‐3 and dependently on dynamin‐related endocytosis, which is involved in cell migra...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464908</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464908</guid>        </item>
        <item>
            <title>Comparative analysis of pre‐replication complex proteins in transformed and normal cells</title>
            <link>http://www.medworm.com/index.php?rid=5464907&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24006</link>
            <description>This study examines the abundance of the major protein constituents of the pre‐replication complex (pre‐RC), both genome‐wide and in association with specific replication origins, namely the lamin B2, c‐myc, 20mer1 and 20mer2 origins. Several pre‐RC protein components, namely ORC1‐6, Cdc6, Cdt1, MCM4, MCM7, as well as additional replication proteins, such as Ku70/86, 14‐3‐3, Cdc45 and PCNA, were comparatively and quantitatively analyzed in both transformed and normal cells. The results show that these proteins are overexpressed and more abundantly bound to chromatin in the transformed compared to normal cells. Interestingly, the 20mer1, 20mer2, and c‐myc origins exhibited a 2‐ to 3‐fold greater origin activity and a 2‐ to 3‐fold greater in vivo association of the ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464907</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464907</guid>        </item>
        <item>
            <title>Leptin regulates estrogen receptor gene expression in ATDC5 cells through the extracellular signal regulated kinase signaling pathway</title>
            <link>http://www.medworm.com/index.php?rid=5464906&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24005</link>
            <description>AbstractBoth estrogen and leptin play an important role in the regulation of physiological processes of endochondral bone formation in linear growth. Estrogen receptors (ERα and ERβ) are known as members of the superfamily of nuclear steroid hormone receptors and are detected in all zones of growth plate chondrocytes. They can be regulated in a ligand‐independent manner. Whether leptin regulates ERs in the growth plate is still not clear. To explore this issue, chondrogenic ATDC5 cells were used in the present study. Messenger RNA and protein analyses were performed by quantitative PCR and western blotting. We found that both ERα and ERβ were dynamically expressed during the ATDC5 cell differentiation for 21 days. Leptin (50ng/ml) significantly upregulated ERα and ERβ mRNA and pr...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464906</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464906</guid>        </item>
        <item>
            <title>Control of mitochondrial activity by miRNAs</title>
            <link>http://www.medworm.com/index.php?rid=5464905&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24004</link>
            <description>AbstractMitochondria supply energy for physiological function and they participate in the regulation of other cellular events including apoptosis, calcium homeostasis and production of reactive oxygen species. Thus, mitochondria play a critical role in the cells. However, dysfunction of mitochondria is related to a variety of pathological processes and diseases. MicroRNAs (miRNAs) are a class of small noncoding RNAs about 22 nucleotides long, and they can bind to the 3' un‐translated region (3'UTR) of mRNAs, thereby inhibiting mRNA translation or promoting mRNA degradation. We summarize the molecular regulation of mitochondrial metabolism, structure and function by miRNAs. Modulation of miRNAs levels may provide a new therapeutic approach for the treatment of mitochondria‐related disea...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464905</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464905</guid>        </item>
        <item>
            <title>The JMJD2A demethylase regulates apoptosis and proliferation in colon cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5464904&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24009</link>
            <description>AbstractJMJD2A is a transcriptional cofactor and enzyme that catalyzes demethylation of histone H3 lysines 9 and 36 and is overexpressed in human tumors, but its role in oncogenesis remains unclear. Here, we show that JMJD2A interacts with the tumor suppressor p53 both in vitro and in HCT116 colon cancer cells. Chromatin immunoprecipitation assays demonstrated that JMJD2A was recruited together with p53 to the promoter of the p21 cell cycle inhibitor upon stimulation with the DNA damaging agent, adriamycin. Downregulation of JMJD2A resulted in increased expression of p21 and of the pro‐apoptotic Puma protein, whereas levels of the anti‐apoptotic Bcl‐2 protein were decreased. Furthermore, JMJD2A knock‐down led to reduced HCT116, DLD‐1 and HT‐29 colon cancer cell proliferation, w...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464904</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464904</guid>        </item>
        <item>
            <title>Hypoxia inhibits the spontaneous calcification of bone marrow‐derived mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5464903&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24014</link>
            <description>In this study, spontaneous calcification of BM‐MSCs from rats was evaluated in normoxia (20% O2) without osteogenic medium after continuous culture for 21 days; obvious mineralized nodules were observed, which were positive for Alizarin Red, collagen‐I (Col‐I), osteocalcin (OC) and alkaline phosphatase (ALP), and mainly consisted of C, O and Ca elements. Interestingly, hypoxia (2% O2) significantly inhibited this spontaneous calcification. In addition, the ALP and calcium content of rBM‐MSCs were sharply reduced. Based on RT‐PCR results, the expression of osteogenic genes (Cbfa1/Runx2, Col‐I, ALP and OC) was reduced compared to that in normoxia. These results demonstrate a natural and unique characterization of rat BM‐MSCs in normoxia after continuous culture and highlight th...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464903</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464903</guid>        </item>
        <item>
            <title>Smile silencing and PMA activation in HeLa cells</title>
            <link>http://www.medworm.com/index.php?rid=5464902&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24013</link>
            <description>AbstractRecent findings indicated that the SMILE gene may be involved in kidney graft tolerance. A microarray study of SMILE knock‐down and PMA activation in HeLa cells was herein used in combination with our earlier analysis based on microarray data of kidney allograft tolerance and rejection in humans and in a rat model. We show that the intersection of the HeLa SMILE knock‐down network with the human tolerance – rejection networks contains two genes, namely XBP1 and ARRB2, recently proven experimentally to be involved in kidney allograft, and one gene, NPHS1, generally involved in kidney function. Also, we show that topological properties of joint SMILE knock‐down – tolerance/rejection and joint PMA activation – tolerance/rejection rat networks are essentially different. J. ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464902</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464902</guid>        </item>
        <item>
            <title>Intratumoral injection of taxol in vivo suppresses A549 tumor showing cytoplasmic vacuolization</title>
            <link>http://www.medworm.com/index.php?rid=5464901&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24012</link>
            <description>In conclusion, high concentration of taxol exhibits a significant anticancer activity by inducing paraptosis‐like cell death in vitro and in vivo, without significant toxicity, suggesting a promising therapeutic strategy for apoptosis‐resistance cancer by inducing ER vacuolization. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464901</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464901</guid>        </item>
        <item>
            <title>Procyanidins from grape pomace are suitable inhibitors of human endothelial NADPH oxidase</title>
            <link>http://www.medworm.com/index.php?rid=5464900&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24011</link>
            <description>AbstractProcyanidins have been associated with a reduced risk of cardiovascular diseases such as atherosclerosis. However, the molecular mechanisms underlying this benefit are not fully understood. Increased reactive oxygen species (ROS) production generated by NADPH oxidase is a common problem in different cardiovascular diseases. Our objective was to evaluate the effects of procyanidin‐rich fractions from distilled grape pomace on NADPH oxidase activity in human umbilical vein endothelial cells (HUVEC). Three differently polymerized and galloylated procyanidin fractions were analysed for their NADPH oxidase inhibitory activity in cell lysates and in HUVEC cultures. All of the three fractions, up to 1 µg/ml, equally inhibited isolated NADPH oxidase in HUVEC lysates in a concentration...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464900</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464900</guid>        </item>
        <item>
            <title>Ca2+ store depletion and endoplasmic reticulum stress are involved in P2X7 receptor‐mediated neurotoxicity in differentiated NG108‐15 cells</title>
            <link>http://www.medworm.com/index.php?rid=5464899&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24010</link>
            <description>In this study, a P2X7R agonist (BzATP) was used to activate P2X7R in differentiated NG108‐15 neuronal cells. In a concentration‐dependent manner, application of BzATP (10‐100 µM) immediately raised cytosolic Ca2+ concentration ([Ca2+]i) and caused cell death after a 24‐h incubation. P2X7R activation for 2 h did not cause cell death but resulted in a sustained reduction in ER Ca2+ pool size, as evidenced by a diminished cyclopiazonic acid‐induced Ca2+ discharge (fura 2 assay) and a lower fluorescent signal in cells loaded with Mag‐fura 2 (ER‐specific Ca2+‐fluorescent dye). Furthermore, P2X7R activation (2 h) led to the appearance of markers of ER stress (phosphorylated α subunit of eukaryotic initiation factor 2 (p‐eIF2α) and C/EBP homologous protein (CHOP)) and a...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5464899</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5464899</guid>        </item>
        <item>
            <title>In vitro model of stromal and epithelial immortalized endometriotic cells</title>
            <link>http://www.medworm.com/index.php?rid=5437065&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24000</link>
            <description>In conclusion, these cells are potentially useful as an experimental model to investigate endometriosis biology. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5437065</comments>
            <pubDate>Wed, 23 Nov 2011 06:40:21 +0100</pubDate>
            <guid isPermaLink="false">5437065</guid>        </item>
        <item>
            <title>Reactivating PP2A by FTY720 as a novel therapy for AML with C‐KIT tyrosine kinase domain mutation</title>
            <link>http://www.medworm.com/index.php?rid=5437068&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24003</link>
            <description>AbstractThe tyrosine kinase domain (TKD) mutations of receptor tyrosine kinase C‐KIT are associated with a poor prognosis in acute myeloid leukemia (AML). However, the underlying mechanisms are not fully understood. We found the activity of Protein phosphatase 2A (PP2A), a human tumor suppressor whose dysfunction contributes to malignant cell behavior, was significantly decreased in AML subgroups harboring C‐KIT/D816V and AML cell line Kasumi‐1 bearing C‐KIT/N822K mutation. Primary AML cells and various AML cell lines were treated with PP2A activator FTY720. FTY720 showed a toxic effect in all leukaemic cells, especially for cells harboring C‐KIT/TKD mutation. Furthermore, FTY720‐induced toxicity in AML leukaemic cells was mediated by restoration of PP2A activity, via down‐re...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5437068</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5437068</guid>        </item>
        <item>
            <title>Targeting radioresistant osteosarcoma cells with parthenolide</title>
            <link>http://www.medworm.com/index.php?rid=5437067&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24002</link>
            <description>AbstractOsteosarcoma is a devastating tumor of bone, primarily affecting adolescents. Osteosarcoma tumors are notoriously radioresistant. Radioresistant cancers, including osteosarcoma, typically exhibit a considerable potential for relapse and development of metastases following treatment. Relapse and metastatic potential can, in part, be due to a specific radioresistant subpopulation of cells with stem‐like characteristics, cancer stem cells, which maintain the capacity to regenerate entire tumors. In the current study, we have investigated whether in vitro treatments with parthenolide, a naturally occurring small molecule that interferes with NF‐κB signaling and has various other effects, will re‐sensitize cancer stem cells and the entire cell population to radiotherapy in osteos...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5437067</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5437067</guid>        </item>
        <item>
            <title>Ascochlorin inhibits growth factor‐induced HIF‐1α activation and tumor‐angiogenesis through the suppression of EGFR/ERK/p70S6K signaling pathway in human cervical carcinoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5437066&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.24001</link>
            <description>AbstractAscochlorin, a non‐toxic prenylphenol compound derived from the fungus Ascochyta viciae, has been shown recently to have anti‐cancer effects on various human cancer cells. However, the precise molecular mechanism of this anti‐cancer activity remains to be elucidated. Here, we investigated the effects of ascochlorin on hypoxia‐inducible factor‐1α (HIF‐1α) and vascular endothelial growth factor (VEGF) expression in human epidermoid cervical carcinoma CaSki cells. Ascochlorin inhibited epidermal growth factor (EGF)‐induced HIF‐1α and VEGF expression through multiple potential mechanisms. First, ascochlorin selectively inhibited HIF‐1α expression in response to EGF stimulation, but not in response to hypoxia (1% O2) or treatment with a transition metal (CoCl2). Se...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5437066</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5437066</guid>        </item>
        <item>
            <title>Molecular chaperones in mammary cancer growth and breast tumor therapy</title>
            <link>http://www.medworm.com/index.php?rid=5437071&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23461</link>
            <description>AbstractHeat shock protein (HSP) levels are elevated in breast cancer and are molecular targets for novel therapies. HSPs were first observed as proteins induced in massive amounts in normal cells exposed to stresses that lead to protein denaturation. Their expanded expression in mammary carcinoma appears to be largely due to the proliferation of malfolded mutant proteins and overexpressed oncoproteins that trigger transcription of HSP genes. HSPs play major roles in malignant transformation and progression mediated through their intrinsic molecular chaperone properties. These permit the emergence of new malignant traits through the facilitated accumulation of altered oncoproteins. The elevation of HSP concentrations in mammary carcinoma is at least partially dependent on heat shock transc...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5437071</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5437071</guid>        </item>
        <item>
            <title>NIP45 negatively regulates RANK ligand induced osteoclast differentiation</title>
            <link>http://www.medworm.com/index.php?rid=5437070&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23460</link>
            <description>In this study, we demonstrate that RANKL treatment down regulates NIP45 expression in mouse bone marrow derived preosteoclast cells. Lentiviral (pGIPZ) mediated shRNA knock‐down of NIP45 expression in RANKL stimulated preosteoclast cells resulted in increased levels of NFATc1, NFATc2 and TRAF6 but not TRAF2 expression compared to control shRNA transduced cells. Also, NIP45 suppression elevated p‐IκB‐α levels and NF‐κB‐luciferase reporter activity. Confocal microscopy demonstrated NIP45 colocalized with TRAF6 in the cytosol of osteoclast progenitor cells. In contrast, RANKL stimulation induced NIP45 nuclear translocation and colocalization with NFATc2 in these cells. Coimmuneprecipitation assasy demonstrated NIP45 binding with NFATc2 but not NFATc1. We further show that shRNA k...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5437070</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5437070</guid>        </item>
        <item>
            <title>Comprehensive analysis of titin protein isoform and alternative splicing in normal and mutant rats</title>
            <link>http://www.medworm.com/index.php?rid=5437069&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23459</link>
            <description>AbstractTitin is a giant protein with multiple functions in cardiac and skeletal muscles. Rat cardiac titin undergoes developmental isoform transition from the neonatal 3.7 MDa N2BA isoform to primarily the adult 2.9 MDa N2B isoform. An autosomal dominant mutation dramatically altered this transformation. Titins from eight skeletal muscles: Tibialis Anterior (TA), Longissimus Dorsi (LD) and Gastrocnemius (GA), Extensor Digitorum Longus (ED), Soleus (SO), Psoas (PS), Extensor Oblique (EO) and Diaphram (DI) were characterized in wild type and in homozygous mutant (Hm) rats with a titin splicing defect. Results showed that the developmental reduction in titin size is eliminated in the mutant rat so that the titins in all investigated skeletal muscles remain large in the adult. The alternative...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5437069</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5437069</guid>        </item>
        <item>
            <title>PI3K/Akt‐dependent functions of TFII‐I transcription factors in mouse embryonic stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5417135&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23441</link>
            <description>AbstractActivation of PI3K/Akt signaling is sufficient to maintain the pluripotency of mouse embryonic stem cells (mESC) and results in down‐regulation of Gtf2i and Gtf2ird1 encoding TFII‐I family transcription factors. To investigate how these genes might be involved in the process of embryonic stem cell differentiation, we performed expression microarray profiling of mESC upon inhibition of PI3K by LY294002. This analysis revealed significant alterations in expression of genes for specific subsets of chromatin‐modifying enzymes. Surprisingly, genome‐wide promoter ChIP‐chip mapping indicated that the majority of differently expressed genes could be direct targets of TFII‐I regulation. The data support the hypothesis that upregulation of TFII‐I factors leads to activation of ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417135</comments>
            <pubDate>Thu, 17 Nov 2011 21:21:28 +0100</pubDate>
            <guid isPermaLink="false">5417135</guid>        </item>
        <item>
            <title>Helicobacter pylori CagA inhibits the expression of Runx3 via Src/MEK/ERK and p38 MAPK pathways in gastric epithelial cell</title>
            <link>http://www.medworm.com/index.php?rid=5417153&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23440</link>
            <description>AbstractInfection with CagA‐positive Helicobacter pylori is the strongest risk factor for gastric carcinoma. Upon delivery into gastric epithelial cells, CagA disturbs cellular functions by physically interacting with and deregulating intracellular signaling molecules via both tyrosine phosphorylation‐dependent and ‐independent mechanisms. Runx3 was suggested to be a tumor suppressor and closely associated with tumorigenesis and progression of gastric cancer. The aim of our study is to verify the effect of H.pylori virulence factor CagA on Runx3 expression level and investigate the corresponding molecular mechanisms and signaling pathways influencing Runx3 expression. Human gastric epithelial immortalized GES‐1 cells were transfected with CagA‐expression vector or control vecto...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417153</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417153</guid>        </item>
        <item>
            <title>Variability of the paracrine‐induced osteoclastogenesis by human breast cancer cell lines</title>
            <link>http://www.medworm.com/index.php?rid=5417152&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23439</link>
            <description>In conclusion, the tested breast cancer cell lines exhibited a high osteoclastogenic potential, although with some variability on the cell response profile, a factor to be considered in the development of new therapeutic approaches for breast cancer‐induced bone metastasis. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417152</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417152</guid>        </item>
        <item>
            <title>Matrix metalloproteinase‐9 in homocysteine‐induced intestinal microvascular endothelial paracellular and transcellular permeability</title>
            <link>http://www.medworm.com/index.php?rid=5417151&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23451</link>
            <description>AbstractAlthough elevated levels of homocysteine (Hcy), known as hyperhomocysteinemia (HHcy), is associated with inflammatory bowel disease, the mechanism of Hcy action is unclear. In the present study we tested the hypothesis that HHcy activates matrix metalloproteinase‐9 (MMP‐9), which in turn enhances permeability of human intestinal microvascular endothelial cell (HIMEC) layer by decreasing expression of endothelial junction proteins and increasing caveolae formation. HIMECs were grown in Transwells and treated with 500 µM Hcy in the presence or absence of MMP‐9 activity inhibitor. Hcy‐induced permeability to FITC‐conjugated bovine serum albumin (FITC‐BSA) was assessed by measuring fluorescence intensity of solutes in the Transwells' lower chambers. The cell‐cell inter...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417151</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417151</guid>        </item>
        <item>
            <title>Inhibition of GPR40 protects MIN6 β‐cells from palmitate‐induced ER stress and apoptosis</title>
            <link>http://www.medworm.com/index.php?rid=5417150&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23450</link>
            <description>In this study, we investigated the possible effects of GPR40 in palmitate‐induced MIN6 β‐cell apoptosis, and found that DC260126, a novel small molecular antagonist of GPR40, could protect MIN6 β‐cells from palmitate‐induced ER stress and apoptosis. Similar results were observed in GPR40‐deficient MIN6 cells, indicating that palmitate‐induced β‐cell apoptosis is at least partially dependent on ER stress pathway via GRP40. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417150</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417150</guid>        </item>
        <item>
            <title>Ins and outs of Mycobacterium tuberculosis PPE family in pathogenesis and implications for novel measures against tuberculosis</title>
            <link>http://www.medworm.com/index.php?rid=5417149&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23449</link>
            <description>AbstractM. tuberculosis is the most successful pathogen with multiple mechanisms to subvert host immune response, resulting in insidious disease. A unique Mycobacterium antigen family termed PPE (Pro‐Pro‐Glu) has long been widely speculated as “molecular mantra” to escape host immunity. Members of this family are characterized by a conserved N terminal and a variable C terminal. This family associated closely with ESAT‐6(ESX) secretion system and largely located in cell wall or cell membrane. The expression of PPE protein is temporally regulated, and highly expressed during M. tuberculosis persistence. Importantly, the distribution of PPE family is so far limited to Mycobacterium genus, prevalent among pathogenic Mycobacterium species. It is tempting to explore this family due to...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417149</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417149</guid>        </item>
        <item>
            <title>Cross‐talk between endothelial and breast cancer cells regulates reciprocal expression of angiogenic factors in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5417148&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23447</link>
            <description>This study demonstrates that the angiogenic activity of malignant mammary epithelial cells is significantly enhanced by the presence of endothelial cells. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417148</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417148</guid>        </item>
        <item>
            <title>Mutagenesis studies of the β I domain metal ion binding sites on integrin αVβ3 ligand binding affinity</title>
            <link>http://www.medworm.com/index.php?rid=5417147&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23448</link>
            <description>AbstractThree divalent cation binding sites in the integrin β I domain have been shown to regulate ligand binding and adhesion. However, the degree of ligand binding and adhesion varies among integrins. The αLβ2 and α4β7 integrins show an increase in ligand binding affinity and adhesion when one of their ADMIDAS (adjacent to MIDAS, or the metal ion‐dependent adhesion site) residues is mutated. By contrast, the α2β1, α5β1, and αIIbβ3 integrins show a decrease in binding affinity and adhesion when their ADMIDAS is mutated. Our study here indicated that integrin αVβ3 had lower affinity when the ADMIDAS was mutated. By comparing the primary sequences of these integrin subunits, we propose that one residue associated with the MIDAS (β3 Ala252) may account for these differences. ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417147</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417147</guid>        </item>
        <item>
            <title>Analysis of the effects of HIV‐1 Tat on the survival and differentiation of vessel wall‐derived mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5417146&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23446</link>
            <description>AbstractHIV infection is an independent risk factor for atherosclerosis development and cardiovascular damage. As vessel wall mesenchymal stem cells (MSCs) are involved in the regulation of vessel structure homeostasis, we investigated the role of Tat, a key factor in HIV replication and pathogenesis, in MSC survival and differentiation. The survival of subconfluent MSCs was impaired when Tat was added at high concentrations (200‐1000 ng/ml), whereas lower Tat concentrations (1‐100 ng/ml) did not promote apoptosis. Tat enhanced the differentiation of MSC toward adipogenesis by the transcription and activity upregulation of PPARγ. This Tat‐related modulation of adipogenesis was tackled by treatment with antagonists of Tat‐specific receptors such as SU5416 and RGD Fc. In contras...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417146</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417146</guid>        </item>
        <item>
            <title>Hypothalamic action of glutamate leads to body mass reduction through a mechanism partially dependent on JAK2</title>
            <link>http://www.medworm.com/index.php?rid=5417145&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23445</link>
            <description>AbstractGlutamate acts in the hypothalamus promoting region‐, and cell‐dependent effects on feeding. Part of these effects are mediated by NMDA receptors, which are up regulated in conditions known to promote increased food intake and thermogenesis, such as exposure to cold and consumption of highly caloric diets. Here, we hypothesized that at least part of the effect of glutamate on hypothalamic control of energy homeostasis would depend on the control of neurotransmitter expression and JAK2 signaling. The expression of NMDA receptors was co‐localized to NPY/AgRP, POMC, CRH and MCH but not to TRH and orexin neurons of the hypothalamus. The acute intracerebroventricular injection of glutamate promoted a dose dependent increase in JAK2 tyrosine phosphorylation. In obese rats, five day...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417145</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417145</guid>        </item>
        <item>
            <title>1α,25(OH)2D3 –dependent modulation of Akt in proliferating and differentiating C2C12 skeletal muscle cells</title>
            <link>http://www.medworm.com/index.php?rid=5417144&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23444</link>
            <description>AbstractWe previously reported that 1α,25‐dihydroxy‐vitamin D3 [1α,25(OH)2D3] induces non‐transcriptional rapid responses through activation of Src and MAPKs in the skeletal muscle cell line C2C12. In the present study we investigated the modulation of Akt by the secosteroid hormone in C2C12 cells at proliferative stage (myoblasts) and at early differentiation stage. In proliferating cells, 1α,25(OH)2D3 activates Akt by phosphorylation in Ser473 in a time‐dependent manner (5‐60 min). When these cells were pre‐treated with methyl‐beta‐cyclodextrin to disrupt caveolae microdomains, hormone‐induced activation of Akt was suppressed. Similar results were obtained by siRNA silencing of caveolin‐1 expression, further indicating that hormone effects on cell membrane cave...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417144</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417144</guid>        </item>
        <item>
            <title>Development, characterization and applications of a novel estrogen receptor beta monoclonal antibody</title>
            <link>http://www.medworm.com/index.php?rid=5417143&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23443</link>
            <description>AbstractThe role of estrogen receptor alpha (ERα) in breast cancer has been studied extensively, and its protein expression is prognostic and a primary determinant of endocrine sensitivity. However, much less is known about the role of ERβ and its relevance remains unclear due to the publication of conflicting reports. Here, we provide evidence that much of this controversy may be explained by variability in antibody sensitivity and specificity and describe the development, characterization and potential applications of a novel monoclonal antibody targeting full‐length human ERβ and its splice variant forms. Specifically, we demonstrate that a number of commercially available ERβ antibodies are insensitive for ERβ and exhibit significant cross‐reaction with ERα. However, our newl...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417143</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417143</guid>        </item>
        <item>
            <title>M‐Ras induces Ral and JNK activation to regulate MEK/ERK‐independent gene expression in MCF‐7 breast cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5417142&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23458</link>
            <description>AbstractConstitutive activation of M‐Ras has previously been reported to cause morphologic and growth transformation of murine cells, suggesting that M‐Ras plays a role in tumorigenesis. Cell transformation by M‐Ras correlated with weak activation of the Raf/MEK/ERK pathway, although contributions from other downstream effectors were suggested. Recent studies indicate that signaling events distinct from the Raf/MEK/ERK cascade are critical for human tumorigenesis. However, it is unknown what signaling events M‐Ras triggers in human cells. Using constitutively active M‐Ras (Q71L) containing additional mutations within its effector binding loop, we found that M‐Ras induces MEK/ERK‐dependent and ‐independent Elk1 activation as well as PI3K/Akt and JNK/cJun activation in human ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417142</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417142</guid>        </item>
        <item>
            <title>MiR‐17‐92 cluster regulates cell proliferation and collagen synthesis by targeting TGFB pathway in mouse palatal mesenchymal cells</title>
            <link>http://www.medworm.com/index.php?rid=5417141&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23457</link>
            <description>AbstractElongation and elevation of palatal shelves, mainly caused by proliferation and extra‐cellular matrix synthesis of palatal mesenchymal cells (PMCs), are essential for normal palatal development. Transforming growth factor beta (TGFB) pathway could induce proliferation inhibition and collagen synthesis in PMCs. Recent studies found that miRNA‐17‐92 (miR‐17‐92) cluster, including miR‐17, miR‐18a, miR‐19a, miR‐20a, miR‐19b, and miR‐92a, expressed in the 1st bronchial arch of mouse embryos during the period of palatal shelf elongation and elevation, and directly targeted TGFB pathway in cancer cell lines. Whether miR‐17‐92 cluster expresses and targets TGFB pathway in PMCs has not yet been studied. Using quantitative real‐time RT‐PCR, we found that miR‐1...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417141</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417141</guid>        </item>
        <item>
            <title>Fluid pressure induces osteoclast differentiation comparably to titanium particles but through a molecular pathway only partly involving TNFα</title>
            <link>http://www.medworm.com/index.php?rid=5417140&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23456</link>
            <description>AbstractIn contrast to the well‐understood inflammatory pathway driven by TNFα, by which implant‐derived particles induce bone resorption, little is known about the process in which loosening is generated as a result of force‐induced mechanical stimulus at the bone‐implant interface. Specifically, there is no knowledge as to what cells or signaling pathways couple mechanical stimuli to bone resorption in context of loosening. We hypothesized that different stimuli i.e. fluid flow versus wear particles, act through different cytokine networks for activation and localization of osteoclasts. By using an animal model in which osteoclasts and bone resorption were induced by fluid pressure or particles, we were able to detect distinct differences in osteoclast localization and inflammat...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417140</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417140</guid>        </item>
        <item>
            <title>Cartilage oligomeric matrix protein enhances matrix assembly during chondrogenesis of human mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5417139&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23455</link>
            <description>AbstractCartilage oligomeric matrix protein/thrombospondin‐5 (COMP/TSP5) is an abundant cartilage extracellular matrix (ECM) protein that interacts with major cartilage ECM components, including aggrecan and collagens. To test our hypothesis that COMP/TSP5 functions in the assembly of the ECM during cartilage morphogenesis, we have employed mesenchymal stem cell (MSC) chondrogenesis in vitro as a model to examine the effects of COMP over‐expression on neo‐cartilage formation. Human bone marrow‐derived MSCs were transfected with either full‐length COMP cDNA or control plasmid, followed by chondrogenic induction in three‐dimensional pellet or alginate‐hydrogel culture. MSC chondrogenesis and ECM production was estimated based on quantitation of sulfated glycosaminoglycan (sGAG)...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417139</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417139</guid>        </item>
        <item>
            <title>Upregulation of recepteur d'origine nantais tyrosine kinase and cell invasiveness via early growth response‐1 in gastric cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5417138&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23454</link>
            <description>AbstractAbnormal accumulation and activation of the recepteur d'origine nantais (RON) has been implicated in carcinogenesis of epithelial tumors. RON expression was induced by the tumor promoter, phorbol 12‐myristate 13‐acetate (PMA), in gastric adenocarcinoma AGS cells. Studies with deleted and site‐directed mutagenesis of Egr‐1 promoter and with expression vectors encoding Egr‐1 confirmed that Egr‐1 is essential for RON expression. In addition, AGS cells pretreated with PMA showed remarkably enhanced invasiveness, which was partially abrogated by siRNA‐targeted RON and Egr‐1. These results suggest that tumor promoter induces RON expression via Egr‐1, which, in turn, stimulates cell invasiveness in AGS cells. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Jou...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417138</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417138</guid>        </item>
        <item>
            <title>Effect of reconstituted discoidal high density lipoproteins on lipid mobilization in RAW 264.7 and CHOK1 cells</title>
            <link>http://www.medworm.com/index.php?rid=5417137&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23453</link>
            <description>AbstractReconstituted discoidal high density lipoproteins (rHDL) resemble nascent HDL, which are formed at the early reverse cholesterol transport steps, and constitute the initial cholesterol (Chol) acceptors from cell membranes. We have used different sized rHDL containing or not Chol, to test their abilities to promote cholesterol and phospholipid efflux from two different cell lines: Raw 264.7 macrophages and CHOK1 cells. All rHDL and lipid‐free apolipoprotein A‐I (apoA‐I) were found to be bound to CHO and RAW cells. In RAW cells, a positive correlation between cellular binding and Chol removal was found for 78 and 96 Å rHDL. Chol‐free rHDL were more effective than Chol‐containing ones in binding to RAW cells and promoting Chol removal. These results were more evident in t...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417137</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417137</guid>        </item>
        <item>
            <title>Apigenin attenuates neointima formation via suppression of vascular smooth muscle cell phenotypic transformation</title>
            <link>http://www.medworm.com/index.php?rid=5417136&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23452</link>
            <description>AbstractAbnormal proliferation, migration and phenotypic modulation of vascular smooth muscle cells (VSMCs) are critical factors in neointima formation during restenosis. The purpose of this study was to determine the efficacy and possible cell signaling mechanisms of apigenin in VSMC activation induced by platelet‐derived growth factor (PDGF)‐BB and injury‐induced neointima formation. Our data revealed a dose‐dependent apigenin inhibition of PDGF‐BB‐induced proliferation of VSMCs by arresting cells in G0/G1‐phase of the cell cycle as determined using 5‐bromo‐2'‐deoxyuridine incorporation and flow cytometry. This was associated with the inhibition of cyclin‐dependent kinase (CDK) 4,6 expression and an increase in p27Kip1 levels in PDGF‐stimulated VSMCs. Moreover, ap...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5417136</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5417136</guid>        </item>
        <item>
            <title>Microarray‐based identification of aminopeptidase N/CD13 target genes in keratinocyte conditioned medium‐stimulated dermal fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=5396426&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23438</link>
            <description>AbstractOf the many processes that affect the outcome of wound repair, epidermal‐dermal interactions are essential to extracellular matrix (ECM) remodeling and in particular, soluble factors released by keratinocytes are known to have a direct impact on the production of ECM by dermal fibroblasts. Aminopeptidase N (APN) has recently been proposed as a cell‐surface receptor for stratifin and is responsible for the stratifin‐mediated matrix metalloproteinase‐1 (MMP‐1) upregulation in fibroblasts. The present study examines whether modulation of APN gene expression has any impact on the fibroblast ECM gene expression profile. The result reveals that in the presence of keratinocyte‐derived soluble factors, transient knockdown of APN in dermal fibroblasts affects the expression of k...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396426</comments>
            <pubDate>Fri, 11 Nov 2011 07:24:13 +0100</pubDate>
            <guid isPermaLink="false">5396426</guid>        </item>
        <item>
            <title>Characterisation and optimisation of a simple, repeatable system for the long term in vitro culture of aligned myotubes in 3D</title>
            <link>http://www.medworm.com/index.php?rid=5396432&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23437</link>
            <description>AbstractIncreased recent research activity in exercise physiology has dramatically improved our understanding of skeletal muscle development and physiology in both health and disease. Advances in bioengineering have enabled the development of biomimetic 3D in vitro models of skeletal muscle which have the potential to further advance our understanding of the fundamental processes that underpin muscle physiology. As the principle structural protein of the extracellular matrix, collagen‐based matrices are popular tools for the creation of such 3D models but the custom nature of many reported systems has precluded their more widespread adoption. Here we present a simple, reproducible iteration of an established 3D in vitro model of skeletal muscle, demonstrating both the high levels of repr...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396432</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5396432</guid>        </item>
        <item>
            <title>Increased expression of the histamine H4 receptor subtype in hypertrophic differentiation of chondrogenic ATDC5 cells</title>
            <link>http://www.medworm.com/index.php?rid=5396431&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23436</link>
            <description>AbstractHistamine has been regarded as an inflammatory mediator of arthritic disorders. We have previously reported that the expression of histamine H4 receptor (H4R) mRNA in synovial tissues was significantly higher in patients with osteoarthritis (OA) compared to those with rheumatoid arthritis. Chondrocyte hypertrophy and endochondral ossification are essential processes in pathologic disorders such as osteophyte formation during OA progression. In the present study, we examined the expression of H4R during differentiation into hypertrophic chondrocytes in the ATDC5 cells, a widely used in vitro model of chondrogenic differentiation. Quantitative reverse transcription polymerase chain reaction showed that the levels of histidine decarboxylase and H4R mRNA on ATDC5 cells were increas...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396431</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5396431</guid>        </item>
        <item>
            <title>Triptolide attenuate the oxidative stress induced by LPS/D‐GalN in mice</title>
            <link>http://www.medworm.com/index.php?rid=5396430&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23434</link>
            <description>AbstractTriptolide, a diterpene triepoxide, is one of the major components of most functional extracts of Tripterygium wilfordii Hook f, which is known to have various biological effects, including immunosuppressive, anti‐inflammatory and anti‐tumor functions. We studied the inhibitory effect of triptolide on endotoxemia (ETM)‐induced oxidative stress, which was induced in C57BL/6 mice by lipopolysaccharide (LPS) and D‐galactosamine (D‐GalN). Pretreatment with triptolide decreased the reactive oxygen species (ROS) levels, mortality rate and liver injury after LPS/D‐GalN injection. We utilized comprehensive proteomics to identify alterations in liver protein expression during pretreatment with triptolide or N‐acetylcysteine (NAC) after LPS/D‐GalN injection, 44 proteins were ...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396430</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5396430</guid>        </item>
        <item>
            <title>BST‐2 binding with cellular MT1‐MMP blocks cell growth and migration via decreasing MMP2 activity</title>
            <link>http://www.medworm.com/index.php?rid=5396429&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23433</link>
            <description>In this study, we provided evidence that both transient and IFN‐α induced BST‐2 could decrease the activity of MMP2 via binding to cellular MT1‐MMP on the C‐ terminus and inhibiting its proteolytic activity; and finally blocking cell growth and migration. Zymography gel and Western‐blot experiments demonstrated that BST‐2 decreased MMP2 activity, but no effect on the expression of MMP2 and MT1‐MMP genes. Confocal and immunoprecipitation data showed that BST‐2 co‐localized and interacted with MT1‐MMP. This interaction inhibited the proteolytic enzyme activity of MT1‐MMP, and blocked the activation of proMMP2. Experimental results of C‐terminus deletion mutant of MT1‐MMP showed that activity of MMP2 was no change and also no interaction existed between the mutant a...</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396429</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5396429</guid>        </item>
        <item>
            <title>In vivo magnetic resonance imaging tracking of SPIO labeled human umbilical cord mesenchymal stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5396428&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23432</link>
            <description>In conclusion, hUC‐MSCs can survive and migrate in the host spinal cord after transplantation, which promote functional recovery after SCI. Noninvasive imaging of transplanted SPIO labeled hUC‐MSCs is feasible. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396428</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5396428</guid>        </item>
        <item>
            <title>Cellular and molecular effects of resveratrol in health and disease</title>
            <link>http://www.medworm.com/index.php?rid=5396427&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.23431</link>
            <description>AbstractResveratrol, a natural polyphenol abundantly found in grape skins and red wine, possesses diverse biochemical and physiological actions, including anti‐inflammatory, anti‐oxidation, anti‐proliferation and promotion of differentiation, and chemopreventive effects. Recently, it is attracting increased attention due to its health benefits, especially in common age‐related diseases such as cardiovascular disease, cancer, type 2 diabetes, and neurological conditions. In this review, we discuss the latest cellular and molecular findings that account for the beneficial actions of resveratrol. J. Cell. Biochem. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396427</comments>
            <pubDate>Mon, 07 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5396427</guid>        </item>
        <item>
            <title>Features: Volume 112, Number 12</title>
            <link>http://www.medworm.com/index.php?rid=5355055&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.22826</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355055</comments>
            <pubDate>Thu, 27 Oct 2011 23:25:58 +0100</pubDate>
            <guid isPermaLink="false">5355055</guid>        </item>
        <item>
            <title>Table of Contents: Volume 112, Number 12</title>
            <link>http://www.medworm.com/index.php?rid=5355054&amp;cid=s_33776_60_f&amp;fid=33776&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcb.22827</link>
            <description>(Source: Journal of Cellular Biochemistry)</description>
            <author>Journal of Cellular Biochemistry</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5355054</comments>
            <pubDate>Thu, 27 Oct 2011 23:25:57 +0100</pubDate>
            <guid isPermaLink="false">5355054</guid>        </item>
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