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        <title>The International Journal of Biochemistry and Cell Biology 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 'The International Journal of Biochemistry and Cell Biology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=The+International+Journal+of+Biochemistry+and+Cell+Biology&t=The+International+Journal+of+Biochemistry+and+Cell+Biology&s=Search&f=source]]></link>
        <lastBuildDate>Sat, 20 Mar 2010 16:01:51 +0100</lastBuildDate>
        <item>
            <title>Endometriosis: new concepts in the pathogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3379650&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20230903%26dopt%3DAbstract</link>
            <description>Authors: Signorile PG, Baldi A
    Endometriosis is a gynecological disease defined by the histological presence of endometrial glands and stroma outside the uterine cavity. Though there are several theories, research scientists remain unsure as to the definitive cause(s) of endometriosis. Considering the relevant health problems caused by endometriosis, all new information on the pathogenesis of this disease, may have important clinical implications. Goal of this article is to summarize the latest advances in the pathogenesis of endometriosis, with particular emphasis on the embryological theory, that has been recently re-proposed. The possible clinical implications of these findings will be discussed.
    PMID: 20230903 [PubMed - as supplied by publisher] (Source: The International Journ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3379650</comments>
            <pubDate>Fri, 12 Mar 2010 00:00:00 +0100</pubDate>
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            <title>Small RNA-mediated gene silencing pathways in C. elegans.</title>
            <link>http://www.medworm.com/index.php?rid=3379654&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20227516%26dopt%3DAbstract</link>
            <description>Authors: Fischer SE
    Small RNA pathways, including the RNA interference (RNAi) pathway and the microRNA (miRNA) pathway, regulate gene expression, defend against transposable elements and viruses, and, in some organisms, guide genome rearrangements. The nematode Caenorhabditis elegans (C. elegans) has been at the forefront of small RNA research; not only were the first miRNAs and their function as regulators of gene expression discovered in C. elegans, but also double-stranded RNA-induced gene silencing by RNAi was discovered in this model organism. Since then, genetic and RNAi-mediated screens, candidate gene approaches, and biochemical studies have uncovered numerous factors in the small RNA pathways and painted a rich palette of interacting pathways. Here we review the different smal...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3379654</comments>
            <pubDate>Thu, 11 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3379654</guid>        </item>
        <item>
            <title>Small RNAs in the animal gonad: Guarding genomes and guiding development.</title>
            <link>http://www.medworm.com/index.php?rid=3379653&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20227517%26dopt%3DAbstract</link>
            <description>Authors: Lau NC
    Germ cells must safeguard, apportion, package, and deliver their genomes with exquisite precision to ensure proper reproduction and embryonic development. Classical genetic approaches have identified many genes controlling animal germ cell development, but only recently have some of these genes been linked to the RNA interference (RNAi) pathway, a gene silencing mechanism centered on small regulatory RNAs. Germ cells contain microRNAs (miRNAs), endogenous siRNAs (endo-siRNAs), and Piwi-interacting RNAs (piRNAs); these are bound by members of the Piwi/Argonaute protein family. piwi genes were known to specify germ cell development, but we now understand that mutations disrupting germline development can also affect small RNA accumulation. Small RNA studies in germ cells ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3379653</comments>
            <pubDate>Thu, 11 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3379653</guid>        </item>
        <item>
            <title>mir-17-92, a cluster of miRNAs in the midst of the cancer network.</title>
            <link>http://www.medworm.com/index.php?rid=3379652&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20227518%26dopt%3DAbstract</link>
            <description>Authors: Olive V, Jiang I, He L
    MicroRNAs (miRNAs) are an abundant class of small non-coding RNAs (ncRNAs) that function to regulate gene expression at the post-transcriptional level. Although their functions were originally described during normal development, miRNAs have emerged as integral components of the oncogenic and tumor suppressor network, regulating nearly all cellular processes altered during tumor formation. In particular, mir-17-92, a miRNA polycistron also known as oncomir-1, is among the most potent oncogenic miRNAs. Genomic amplification and elevated expression of mir-17-92 were both found in several human B-cell lymphomas, and its enforced expression exhibits strong tumorigenic activity in multiple mouse tumor models. mir-17-92 carries out pleiotropic functions during...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3379652</comments>
            <pubDate>Thu, 11 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3379652</guid>        </item>
        <item>
            <title>N-Domain of human adhesion/growth-regulatory galectin-9: preference for distinct conformers and non-sialylated N-glycans and detection of ligand-induced structural changes in crystal and solution.</title>
            <link>http://www.medworm.com/index.php?rid=3379651&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20227520%26dopt%3DAbstract</link>
            <description>Authors: Sol&amp;#xED;s D, Mat&amp;#xE9; MJ, Lohr M, Ribeiro JP, L&amp;#xF3;pez-Merino L, Andr&amp;#xE9; S, Buzamet E, Ca&amp;#xF1;ada FJ, Kaltner H, Lensch M, Mart&amp;#xED;n-Ruiz F, Haroske G, Wollina U, Kloor M, Kopitz J, S&amp;#xE1;iz JL, Men&amp;#xE9;ndez M, Jim&amp;#xE9;nez-Barbero J, Romero A, Gabius HJ
    Human tandem-repeat-type galectin-9 is a potent adhesion/growth-regulatory effector via lectin capacity of its N- and C-terminal domains. This bioactivity prompted further crystallographic study of the N-domain, combined with analysis in solution. Binding of lactose markedly increased the N-domain's resistance to thermal denaturation. Crystallography revealed its intimate contact profile, besides detecting an extension of the beta-sandwich fold by an antiparallel beta-strand F0 aligned to the C-terminal F1 strand. ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3379651</comments>
            <pubDate>Thu, 11 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3379651</guid>        </item>
        <item>
            <title>The Road Toward microRNA Therapeutics.</title>
            <link>http://www.medworm.com/index.php?rid=3379649&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20227519%26dopt%3DAbstract</link>
            <description>Authors: Seto AG
    Within the last fifteen years, microRNAs (miRNAs) have emerged as powerful regulators of gene expression. Highly conserved, these small RNAs appear to regulate nearly every aspect of eukaryotic biology. Perturbation of miRNA expression has been correlated with cancer and, more recently, a variety of diseases; however, the more striking observation is that manipulation of miRNA levels can control disease phenotypes. Hence, the race to bring the first miRNA therapeutic to the market has begun. This review provides an overview of the history and mechanism of miRNAs, the ongoing efforts to develop miRNA therapies, and the nucleic acid technologies that may be key to the success of a miRNA therapeutic.
    PMID: 20227519 [PubMed - as supplied by publisher] (Source: The Inte...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3379649</comments>
            <pubDate>Thu, 11 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3379649</guid>        </item>
        <item>
            <title>Tricyclic antidepressants and mecamylamine bind to different sites in the human alpha4beta2 nicotinic receptor ion channel.</title>
            <link>http://www.medworm.com/index.php?rid=3361678&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20223294%26dopt%3DAbstract</link>
            <description>In conclusion, our data indicate that tricyclic antidepressants and mecamylamine efficiently inhibit the ion channel by interacting at different luminal sites. The high proportion of protonated mecamylamine calculated at physiological pH suggests that this drug can be attracted to the channel mouth before binding deeper within the receptor ion channel finally blocking ion flux.
    PMID: 20223294 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3361678</comments>
            <pubDate>Mon, 08 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3361678</guid>        </item>
        <item>
            <title>Human intestinal MUC17 mucin augments intestinal cell restitution and enhances healing of experimental colitis.</title>
            <link>http://www.medworm.com/index.php?rid=3354535&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20211273%26dopt%3DAbstract</link>
            <description>Authors: Luu Y, Junker W, Rachagani S, Das S, Batra SK, Heinrikson RL, Shekels LL, Ho SB
    The membrane-bound mucins, MUC17 (human) and Muc3 (mouse), are highly expressed on the apical surface of intestinal epithelia and are thought to be cytoprotective. The extracellular regions of these mucins contain EGF-like Cys-rich segments (CRD1 and CRD2) connected by an intervening linker domain (L). The purpose of this study was to determine the functional activity of human MUC17 membrane-bound mucin. Methods: Endogenous MUC17 was inhibited in LS174T colon cells by stable transfection of a small hairpin RNA targeting MUC17 (LSsi cells). The effect of recombinant MUC17-CRD1-L-CRD2 protein on migration, apoptosis, and experimental colitis was determined. Results: Reduced MUC17 expression in LSsi c...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3354535</comments>
            <pubDate>Fri, 05 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3354535</guid>        </item>
        <item>
            <title>Selective and potent furin inhibitors protect cells from anthrax without significant toxicity.</title>
            <link>http://www.medworm.com/index.php?rid=3336025&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20197107%26dopt%3DAbstract</link>
            <description>Authors: Remacle AG, Gawlik K, Golubkov VS, Cadwell GW, Liddington RC, Cieplak P, Millis SZ, Desjardins R, Routhier S, Yuan XW, Neugebauer WA, Day R, Strongin AY
    Furin and related proprotein convertases cleave the multibasic motifs R-X-R/K/X-R in the precursor proteins and, as a result, transform the latent proproteins into biologically active proteins and peptides. Furin is present both in the intracellular secretory pathway and at the cell surface. Intracellular furin processes its multiple normal cellular targets in the Golgi and secretory vesicle compartments while cell-surface furin appears to be essential only for the processing of certain pathogenic proteins and, importantly, anthrax. To design potent, safe and selective inhibitors of furin, we evaluated the potency and selectiv...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3336025</comments>
            <pubDate>Sat, 27 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3336025</guid>        </item>
        <item>
            <title>Crosstalk between desmoglein-2/desmocollin-2/Src kinase and, coxsackie and adenovirus receptor/ZO-1 protein complexes, regulates blood-testis barrier dynamics.</title>
            <link>http://www.medworm.com/index.php?rid=3327995&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20188849%26dopt%3DAbstract</link>
            <description>This study aims to fill this gap with the functional investigation of two desmosomal cadherins, desmoglein-2 and desmocollin-2, by their specific knockdown in Sertoli cells cultured in vitro. Reminiscent of the blood-testis barrier in vivo, desmosome-like structures were visible by electron microscopy when Sertoli cells were cultured at high density, thereby forming a polarized epithelium with functional cell junctions. At this point, we opted to focus our efforts on desmoglein-2 and desmocollin-2 based on results which illustrated desmosomal mRNAs to be expressed by Sertoli and germ cells, as well as on results which illustrated desmoglein-2 to co-immunoprecipitate with plakoglobin, c-Src and desmocollin-2. Simultaneous knockdown of desmoglein-2 and desmocollin-2 not only led to a reducti...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3327995</comments>
            <pubDate>Wed, 24 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3327995</guid>        </item>
        <item>
            <title>&quot;Enhanced proliferation and migration of vascular smooth muscle cells in response to vascular injury under hyperglycemic conditions is controlled by beta3 integrin signaling&quot;</title>
            <link>http://www.medworm.com/index.php?rid=3318932&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20184965%26dopt%3DAbstract</link>
            <description>Authors: Panchatcharam M, Miriyala S, Yang F, Leitges M, Chrzanowska-Wodnicka M, Quilliam LA, Anaya P, Morris AJ, Smyth SS
    Atheroma formation and restenosis following percutaneous vascular intervention involve the growth and migration of vascular smooth muscle cells (SMCs) into neointimal lesions, in part due to changes in the extracellular matrix. While some clinical studies have suggested that, in comparison to non-diabetics, beta3 integrin inhibition in diabetic patients confers protection from restenosis, little is known regarding the role of beta3 integrin inhibition on SMC responses in this context. To understand the molecular mechanisms underlying integrin-mediated regulation of SMC function in diabetes, we examined SMC responses in diabetic mice deficient in integrin beta3 and ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3318932</comments>
            <pubDate>Mon, 22 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3318932</guid>        </item>
        <item>
            <title>Molecular regulation of Nogo-A in neural cells: novel insights into structure and function.</title>
            <link>http://www.medworm.com/index.php?rid=3302815&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20171301%26dopt%3DAbstract</link>
            <description>Authors: Bongiorno D, Petratos S
    Nogo-A is part of the Reticulon family of proteins localized to the myelin and oligodendroglial plasma membranes. Nogo-A specifically initiates signal transduction cascades limiting axonal regrowth following injury and disease in the adult mammalian central nervous system (CNS). Recent novel data support the contention that neuronal Nogo-A plays an important role in regulating cytoskeletal re-organization without the requirement of signaling through its cognate receptor (Nogo Receptor). These data, along with the recent findings that the N-terminus of Nogo-A can interact with integrins and the amyloid precursor protein extracellularly, as well as ubiquitin ligases intracellularly add a layer of complexity to its functional role in the CNS.
    PMID: 201...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3302815</comments>
            <pubDate>Wed, 17 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3302815</guid>        </item>
        <item>
            <title>Neuronal Apoptosis Inhibitory protein, NAIP, is an Inhibitor of Procaspase-9.</title>
            <link>http://www.medworm.com/index.php?rid=3302814&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20171302%26dopt%3DAbstract</link>
            <description>Authors: Davoodi J, Ghahremani MH, Es-Haghi A, Mohammad-Gholi A, Mackenzie A
    Ability of the full length NAIP and its BIR3 domain in inhibition of the proteases of the intrinsic apoptosis pathway was investigated. Activity of endogenous executioner caspases was drastically reduced by both recombinant NAIP BIR3 (NBIR3) as well as the full length protein. Western blotting experiments showed that the full length NAIP and its BIR3 domain inhibited the cleavage of procaspase-3 by apoptosome activated caspase-9. Moreover, full length NAIP inhibited autocatalytic processing of procaspase-9 in the Apoptosome complex indicating that unlike other Inhibitor of Apoptosis Proteins (IAPs) human NAIP is an inhibitor of procaspase-9. Furthermore, inhibition of single-chain caspase-9 (human caspase-9, D...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3302814</comments>
            <pubDate>Wed, 17 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3302814</guid>        </item>
        <item>
            <title>Peroxisome proliferator-activated receptors gamma reverses hepatic nutritional fibrosis in mice and suppresses activation of hepatic stellate cells in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3291281&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20156580%26dopt%3DAbstract</link>
            <description>In conclusion, the present study shows that MCD diet-induced fibrosing steatohepatitis can be reversed by overexpression of PPARgamma. It is likely that PPARgamma reverses fibrosis by reducing HSCs proliferation, inducing cell cycle arrest and apoptosis.
    PMID: 20156580 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3291281</comments>
            <pubDate>Fri, 12 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3291281</guid>        </item>
        <item>
            <title>Pyruvate kinase type M2: a key regulator of the metabolic budget system in tumor cells.</title>
            <link>http://www.medworm.com/index.php?rid=3291280&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20156581%26dopt%3DAbstract</link>
            <description>Authors: Mazurek S
    Cell proliferation only proceeds when metabolism is capable of providing a budget of metabolic intermediates that is adequate to ensure both energy regeneration and the synthesis of cell building blocks in sufficient amounts. In tumor cells, the glycolytic pyruvate kinase isoenzyme M2 determines whether glucose is converted to lactate for regeneration of energy (active tetrameric form, Warburg effect) or used for the synthesis of cell building blocks (nearly inactive dimeric form). This review discusses the regulation mechanisms of pyruvate kinase M2 expression by different transcription factors as well as the regulation of pyruvate kinase M2 activity by direct interaction with certain oncoproteins, tyrosine and serine phosphorylation, binding of phosphotyrosine pept...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3291280</comments>
            <pubDate>Fri, 12 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3291280</guid>        </item>
        <item>
            <title>Hexafluoroisopropanol-induced helix-sheet transition of stem bromelain: correlation to function.</title>
            <link>http://www.medworm.com/index.php?rid=3291279&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20156582%26dopt%3DAbstract</link>
            <description>This study demonstrates that hexafluoroisopropanol can induce a conformational change in stem bromelain to a form with potentially useful therapeutic properties different from those of the native protein.
    PMID: 20156582 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3291279</comments>
            <pubDate>Fri, 12 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3291279</guid>        </item>
        <item>
            <title>International Journal of Biochemistry and Cell Biology.</title>
            <link>http://www.medworm.com/index.php?rid=3267794&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20149891%26dopt%3DAbstract</link>
            <description>Authors: Gilroy DW
    
    PMID: 20149891 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3267794</comments>
            <pubDate>Mon, 08 Feb 2010 00:00:00 +0100</pubDate>
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            <title>MicroRNAs in Immune Regulation-Opportunities for Cancer Immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=3262543&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20144731%26dopt%3DAbstract</link>
            <description>Authors: Okada H, Kohanbash G, Lotze MT
    Endogenously produced microRNAs are predicted to regulate the translation of over two-thirds all human gene transcripts. Certain microRNAs regulate expression of genes that are critically involved in both innate and adaptive immune responses. Immune cells represent a highly attractive target for microRNA gene therapy approaches, as these cells can be isolated, treated and then reintroduced into the patient. In this short review, we discuss how recent discoveries on the roles of microRNAs in immune-regulation will advance the field of cancer immunology and immunotherapy. Targets identified already in T cells include microRNAs, miR-17-92 family, miR-155, and miR-181a. In macrophages, miR-125b, miR-146, and miR-155 act as Pathogen Associated Molecul...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3262543</comments>
            <pubDate>Fri, 05 Feb 2010 00:00:00 +0100</pubDate>
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        <item>
            <title>Mechanisms of inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=3254904&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20138153%26dopt%3DAbstract</link>
            <description>Authors: Kargul J, Laurent GJ
    
    PMID: 20138153 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3254904</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3254904</guid>        </item>
        <item>
            <title>Metabolic interplay between intra- and extra-cellular uridine metabolism via an atp driven uridine-utp cycle in brain.</title>
            <link>http://www.medworm.com/index.php?rid=3236597&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20117232%26dopt%3DAbstract</link>
            <description>METABOLIC INTERPLAY BETWEEN INTRA- AND EXTRA-CELLULAR URIDINE METABOLISM VIA AN ATP DRIVEN URIDINE-UTP CYCLE IN BRAIN.
    Int J Biochem Cell Biol. 2010 Jan 28;
    Authors: Ipata PL, Barsotti C, Tozzi MG, Camici M, Balestri F
    Uridine, a pyrimidine nucleoside essential for the synthesis of RNA and biomembranes, has several trophic functions in the central nervous system, that involve a physiological regulation of pyrimidine nucleotides and phospholipids content, and a maintenance of brain metabolism under ischemia, or pathological situations. The understanding of uridine production in the brain is therefore of fundamental importance. Brain has a limited capacity to synthesize ex novo the pyrimidine ring, and a reasonable source of brain uridine is UTP. The kinetics of UTP breakdown, as...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3236597</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3236597</guid>        </item>
        <item>
            <title>Nitric oxide mediates distinct effects of various LPS chemotypes on phagocytosis and leukotriene synthesis in human neutrophils.</title>
            <link>http://www.medworm.com/index.php?rid=3236596&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20117233%26dopt%3DAbstract</link>
            <description>Authors: Zagryazhskaya AN, Lindner SC, Grishina ZV, Galkina SI, Steinhilber D, Sud'ina GF
    We investigated the effect of lipopolysaccharide (LPS) chemotypes differing in their carbohydrate chain length on phagocytosis of serum-opsonized zymosan (OZ) particles and related functions of human polymorphonuclear leukocyte (PMNL, neutrophils). LPS from deep-core mutant (Re), complete-core (Ra) and smooth (S) phenotypes of Salmonella typhimurium were studied. Priming of neutrophils with various LPSs caused prominent enhancement of OZ phagocytosis, superoxide production and leukotriene (LT) synthesis in neutrophils, with LPS effects increasing as Re&amp;lt;S&amp;lt;Ra. The LPS forms were less potent to activate OZ uptake in the presence of MK-886, 5-lipoxygenase activating protein inhibitor, suggesting...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3236596</comments>
            <pubDate>Thu, 28 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3236596</guid>        </item>
        <item>
            <title>Oncogenic RAS alters the global and gene specific Histone modification pattern during Epithelial - Mesenchymal Transition in colorectal carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3223878&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20109579%26dopt%3DAbstract</link>
            <description>We report that these two genes demonstrate matching inverse histone repression patterns on their promoter, while histone markers associated with an active state of genes were affected by the RAS activated signalling pathway MEK-ERK-MSK1. Furthermore, we show that though the level of methyltransferases enzymes was increased, the status of H3 three-methylation at lysine 27 (H3K27me(3)), associated with gene repression on the promoter of Cyclin D1, was lower. Together, these results suggest that histone covalent modifications can be affected by oncogenic RAS pathways to regulate the expression of target genes like Cyclin D1 or E-cadherin and that the dynamic balance of opposing histone modifying enzymes is critical for the regulation of cell proliferation.
    PMID: 20109579 [PubMed - as supp...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3223878</comments>
            <pubDate>Mon, 25 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3223878</guid>        </item>
        <item>
            <title>The plasma membrane Ca(2+)-ATPase: regulation by PSD-95/Dlg/Zo-1 scaffolds.</title>
            <link>http://www.medworm.com/index.php?rid=3212682&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20100590%26dopt%3DAbstract</link>
            <description>Authors: Kruger WA, Monteith GR, Poronnik P
    Since its first characterization in the erythrocyte membrane the plasma membrane Ca(2+)-ATPase has been well-defined as a ubiquitous mechanism for the efflux of Ca(2+) from eukaryotic cells. With 4 isoforms and potentially 30 splice variants, defining the absolute physiological role of plasma membrane Ca(2+)-ATPase has been difficult and very limited due to the lack of effective blockers/antibodies and difficulties in measuring the activity of individual isoforms. This review highlights recent developments showing that specific plasma membrane Ca(2+)-ATPase isoforms are subject to dynamic regulation by PSD-95/Dlg/Zo-1 scaffold proteins. Such interactions support a new paradigm, that by serving as key players in multifunctional protein complex...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3212682</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3212682</guid>        </item>
        <item>
            <title>Human beta-defensin 1: a restless warrior against allergies, infections and cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3212681&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20100591%26dopt%3DAbstract</link>
            <description>Authors: Oca EP
    Human beta-defensin 1 (hBD-1) is probably the most important antimicrobial peptide in epithelial tissues. Its alleles and/or altered gene expression have been associated with at least twenty human diseases. hBD-1 is a tumor suppressor and DEFB1 is the only innate immunity gene that shows long-term balanced selection and heterozygote advantage. It is unique in its constitutive expression, but is still capable of upregulation upon inflammatory or microbial stimuli. The present minireview focuses on hBD-1 properties, biological function, its proposed pathogenic mechanisms and the potential uses of elicitors, inhibitors or the peptide itself in the treatment of hBD-1-related human diseases including allergies, infections and cancer.
    PMID: 20100591 [PubMed - as supplied ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3212681</comments>
            <pubDate>Fri, 22 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3212681</guid>        </item>
        <item>
            <title>Modulation of the Zac1's transactivation and coactivation functions via PML and Daxx within distinct subcellular localizations.</title>
            <link>http://www.medworm.com/index.php?rid=3212684&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097304%26dopt%3DAbstract</link>
            <description>Authors: Ho CL, Huang YC, Tai CK, Liu ST, Wang JK, Wang WM, Huang SM
    Zac1 acts as a transcription factor and a transcriptional cofactor cooperated with histone acetyltransferases and/or histone deacetylases. The molecular mechanisms underlying the subcellular localization and specificity of Zac1 transcriptional regulation are unclear. Here, we show that Zac1 might have physical and functional interactions with death-associated protein (Daxx) and promyelocytic leukemia protein (PML). However, unlike Daxx, nuclear Zac1 was not relocalized into PML nuclear bodies (PML-NBs). The enhancement of the transactivation activity of Zac1 by PML and Daxx might occur outside PML-NBs. Other components of PML-NBs, such as CREB-binding protein (CBP), ubiquitin-conjugating enzyme 9, and p53, were also r...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3212684</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3212684</guid>        </item>
        <item>
            <title>SMAR1 regulates free radical stress through modulation of AKR1a4 enzyme activity.</title>
            <link>http://www.medworm.com/index.php?rid=3212683&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20097305%26dopt%3DAbstract</link>
            <description>Authors: Singh S, Sreenath K, Pavithra L, Roy S, Chattopadhyay S
    Tumor suppressor SMAR1 is known to be involved in regulation of cell cycle and apoptotic genes transcription. It also directly interacts and stabilizes p53 through phosphorylation at serine-15 residue. Although the functions of SMAR1 are mainly restricted to the nucleus, we report its novel function with the cytoplasm. We show that SMAR1 directly interacts and inhibits AKR1a4 enzyme activity. Interestingly, AKR1a4 enzyme activity is elevated in higher grades of breast cancer where SMAR1 expression is drastically downregulated. Higher AKR1a4 activity protects the cancer cells from anticancer drugs and free radical stress. Through increased metabolism, ARK1a4 helps fulfilling higher energy needs required by cancer cell. The...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3212683</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3212683</guid>        </item>
        <item>
            <title>PPIase domain of trigger factor acts as auxiliary chaperone site to assist the folding of protein substrates bound to the crevice of trigger factor.</title>
            <link>http://www.medworm.com/index.php?rid=3212685&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20096367%26dopt%3DAbstract</link>
            <description>Authors: Liu CP, Zhou QM, Fan DJ, Zhou JM
    Trigger factor (TF) is the first chaperone encountered by nascent chains in bacteria, which consists of two modules: peptidyl-prolyl-cis/trans-isomerase (PPIase) domain and a crevice built by both N- and C- terminal domains. While the crevice is suggested to provide a protective space over the peptide exit site of ribosome for nascent polypeptides to fold, it remains unclear whether PPIase domain is directly involved in assisting protein folding. Here, we introduced structural change into different regions of TF, and investigated their influence on the chaperone function of TF in assisting the folding of various substrate proteins, including oligomeric glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and monomeric carbonic anhydrase II (CA II) ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3212685</comments>
            <pubDate>Tue, 19 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3212685</guid>        </item>
        <item>
            <title>Lipopolysaccharide-induced inhibition of connexin43 gap junction communication in astrocytes is mediated by downregulation of caveolin-3.</title>
            <link>http://www.medworm.com/index.php?rid=3200952&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20093193%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effect of lipopolysaccharide (LPS) on connexin43 (Cx43) gap junctions in rat primary astrocytes. Following LPS treatment, dose- and time-dependent inhibition of Cx43 expression was seen. Moreover, LPS induced a reduction in Cx43 immunoreactivity at cell-cell contacts and significantly inhibited GJIC, as revealed by the fluorescent dye scrape loading assay. Toll-like receptor 4 (TLR4) protein expression was increased 2- to 3-fold following LPS treatment. To study the pathways underlying these LPS-induced effects, we examined downstream effectors of TLR4 signaling and found that LPS induced a significant increase in phosphorylated extracellular signal-regulated kinase (pERK) levels up to 6h, followed by signal attenuation and downregulation of caveolin-3 ex...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3200952</comments>
            <pubDate>Mon, 18 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3200952</guid>        </item>
        <item>
            <title>Glycation of PDGF results in decreased biological activity.</title>
            <link>http://www.medworm.com/index.php?rid=3194519&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083221%26dopt%3DAbstract</link>
            <description>Authors: Nass N, Vogel K, Hofmann B, Presek P, Silber RE, Simm A
    Advanced glycation end products (AGEs) are formed by the non enzymatic glycation of proteins by reducing carbohydrates or alpha-oxoaldehydes such as glyoxal and methylglyoxal and further rearrangements, eliminations and oxidations. AGE-modifications alter peptide structure, function and stability and accumulate under several pathophysiological conditions such as diabetes and are considered a biomarker of ageing. PDGF is a major regulator of wound healing, which is impaired in hyperglycaemia and ageing. We analysed whether glycated PDGF has impaired activity in cell culture models and occurs in human subjects. PDGF was AGE-modified by the alpha-oxoaldehydes glyoxal and methylglyoxal, which was shown by western blotting usi...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3194519</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3194519</guid>        </item>
        <item>
            <title>Immunoglobulin-like cell adhesion molecules: novel signaling players in epithelial ovarian cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3194518&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083222%26dopt%3DAbstract</link>
            <description>This article will discuss the signaling function of immunoglobulin-like cell adhesion molecules in the context of ovarian cancer progression, an issue that, on one hand, will shed light on novel pathogenic mechanisms and, on the other hand, may offer viable therapeutic targets for such a devastating disease.
    PMID: 20083222 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3194518</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3194518</guid>        </item>
        <item>
            <title>Periostin expression distinguishes between light and dark hypertrophic chondrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3194517&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083223%26dopt%3DAbstract</link>
            <description>Authors: Chen KS, Tatarczuch L, Mirams M, Ahmed YA, Pagel CN, Mackie EJ
    Hypertrophic chondrocytes exist in two forms detectable by electron microscopy, light and dark chondrocytes; the functional implications of the heterogeneous morphology are unknown. The aims of the study were to establish a method for separating light from dark hypertrophic chondrocytes and to identify genes differentially expressed between the two populations. Three-dimensional pellet cultures of chondrocytes from cartilage of neonatal rats were induced to undergo hypertrophy by treatment with triiodothyronine. Cultures were dissociated and subjected to density gradient centrifugation. The cell fraction with the lowest density comprised predominantly light hypertrophic chondrocytes, and the fraction with the highe...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3194517</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3194517</guid>        </item>
        <item>
            <title>Radical sequestration by protein-bound 3,4-dihydroxyphenylalanine.</title>
            <link>http://www.medworm.com/index.php?rid=3194516&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083224%26dopt%3DAbstract</link>
            <description>Authors: Nelson M, Foxwell AR, Tyrer P, Dean RT
    Protein-bound 3,4-dihydroxyphenylalanine (PB-DOPA), a redox-active product of protein oxidation, is capable of functioning as both a pro- and antioxidant. A number of in vitro and in vivo studies have demonstrated a toxic, non-toxic or even beneficial effect of free DOPA, however little investigation has examined the physiological activity of PB-DOPA. Being the major treatment available for Parkinson's disease, most studies have focused on the effect of DOPA within neurological cells or tissues, although the presence of PB-DOPA in other locations, for example within atherosclerotic plaques, suggests that broader research is needed to fully understand the physiological effects of both free and PB-DOPA. We hypothesise that the generation of...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3194516</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3194516</guid>        </item>
        <item>
            <title>MicroRNAs in Ovarian Cancer Biology and Therapy Resistance.</title>
            <link>http://www.medworm.com/index.php?rid=3194515&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083225%26dopt%3DAbstract</link>
            <description>Authors: van Jaarsveld MT, Helleman J, Berns EM, Wiemer EA
    Epithelial ovarian cancer is the most common cause of death from gynecological malignancies in the Western world. The overall 5-year survival is only 30% due to late diagnosis and development of resistance to chemotherapy. There is, therefore, a strong need for prognostic and predictive markers to help optimize and personalize treatment hence ameliorating the prognosis of ovarian cancer patients. Since 2006, an increasing number of studies have indicated an essential role for microRNAs in ovarian cancer tumorigenesis. In this review, we provide an overview of the microRNAs that have been associated with different aspects of ovarian cancer, such as tumor subtype, stage, histological grade, germline mutations in BRCA genes, progn...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3194515</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3194515</guid>        </item>
        <item>
            <title>Subcellular localization of ribosomal p0-like protein mrt4 is determined by its n-terminal domain.</title>
            <link>http://www.medworm.com/index.php?rid=3194514&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20083226%26dopt%3DAbstract</link>
            <description>In this report we investigated the biological nature of the human Mrt4 protein. First, we constructed a series of hybrid hMrt4-P0 proteins by replacing various domains of the P0 protein with corresponding protein fragments from hMrt4. We found that hMrt4 binds to the same site on the large ribosomal subunit as does P0, but despite the sequence homology it is not able to functionally complement the lack of P0. Using fluorescence microscopy and biochemical approaches we also show that hMrt4 occupies predominantly the nucleolar compartment, in contrast to P0 and P1/P2, which are located in the cytoplasm. The nucleolar accumulation of hMrt4 does not depend on a specific nucleolus localization signal, but rather occurs via interaction with established nucleolar components such as rRNA; however,...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3194514</comments>
            <pubDate>Fri, 15 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3194514</guid>        </item>
        <item>
            <title>Nlrp3: An immune sensor of cellular stress and infection.</title>
            <link>http://www.medworm.com/index.php?rid=3186202&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20079456%26dopt%3DAbstract</link>
            <description>Authors: Lamkanfi M, Kanneganti TD
    Innate immune cells rely on pathogen recognition receptors such as the nucleotide-binding and oligomerization domain (NOD)-like receptor (NLR) family to mount an appropriate immune response against microbial threats. The NLR protein Nlrp3 senses microbial ligands, endogenous danger signals and crystalline substances in the cytosol to trigger the assembly of a large caspase-1-activating protein complex termed the Nlrp3 inflammasome. Autoproteolytic maturation of caspase-1 zymogens in the Nlrp3 inflammasome leads to maturation and extracellular release of the pro-inflammatory cytokines interleukin (IL)-1beta and IL-18. Gain-of-function mutations in the NOD domain of Nlrp3 are associated with auto-inflammatory disorders characterized by skin rashes and p...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186202</comments>
            <pubDate>Thu, 14 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186202</guid>        </item>
        <item>
            <title>Model systems and experimental conditions that lead to effective repopulation of the liver by transplanted cells.</title>
            <link>http://www.medworm.com/index.php?rid=3186199&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080205%26dopt%3DAbstract</link>
            <description>MODEL SYSTEMS AND EXPERIMENTAL CONDITIONS THAT LEAD TO EFFECTIVE REPOPULATION OF THE LIVER BY TRANSPLANTED CELLS.
    Int J Biochem Cell Biol. 2010 Jan 14;
    Authors: Shafritz DA, Oertel M
    In recent years, there has been substantial progress in transplanting cells into the liver with the ultimate goal of restoring liver mass and function in both inherited and acquired liver diseases. The basis for considering that this might be feasible is that the liver is a highly regenerative organ. After massive liver injury or surgical removal of two-thirds or more of the liver tissue, the organ can restore its mass with completely normal morphologic structure and function. It has also been found under highly selective conditions that transplanted hepatocytes can fully repopulate the liver and c...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186199</comments>
            <pubDate>Thu, 14 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186199</guid>        </item>
        <item>
            <title>Oligomerization conditions Mdm2-mediated efficient p53 poly-ubiquitylation but not its proteasomal degradation.</title>
            <link>http://www.medworm.com/index.php?rid=3186198&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20080206%26dopt%3DAbstract</link>
            <description>Authors: Hjerpe R, Aillet F, Lopitz-Otsoa F, Lang V, Torres-Ramos M, Farr&amp;#xE1;s R, Hay RT, Rodr&amp;#xED;guez MS
    In normal cells p53 is maintained at low level through the action of the Ubiquitin-Proteasome System. As a consequence of p53 transcriptional activity, various regulators of this tumor suppressor are produced, forming a negative feedback loop tightly controlling p53 stability. One of the most prominent is the ubiquitin-ligase Mdm2. Here, we have used a transfer of signals strategy to study the p53 degradation process promoted by Mdm2 in the absence of p53-transcriptional activity. Our results show that in a p53 null background, transcriptionally silent p53-fusions require multiple N- and C-terminal signals to be optimally targeted to proteasomal degradation. As for WT p53, p53-...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186198</comments>
            <pubDate>Thu, 14 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186198</guid>        </item>
        <item>
            <title>Inhibitory mechanisms and binding site location for serotonin selective reuptake inhibitors on nicotinic acetylcholine receptors.</title>
            <link>http://www.medworm.com/index.php?rid=3186201&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20079457%26dopt%3DAbstract</link>
            <description>Authors: Arias HR, Feuerbach D, Bhumireddy P, Ortells MO
    Functional and structural approaches were used to examine the inhibitory mechanisms and binding site location for fluoxetine and paroxetine, two serotonin selective reuptake inhibitors, on nicotinic acetylcholine receptors (AChRs) in different conformational states. The results establish that: (a) fluoxetine and paroxetine inhibit halpha1beta1gammadelta AChR-induced Ca(2+) influx with higher potencies than dizocilpine. The potency of fluoxetine is increased approximately 10-fold after longer pre-incubation periods, which is in agreement with the enhancement of [(3)H]cytisine binding to resting but activatable Torpedo AChRs elicited by these antidepressants, (b) fluoxetine and paroxetine inhibit the binding of the phencyclidine an...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186201</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186201</guid>        </item>
        <item>
            <title>Molecules in Focus ERp57, a multifunctional endoplasmic reticulum resident oxidoreductase.</title>
            <link>http://www.medworm.com/index.php?rid=3186200&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20079872%26dopt%3DAbstract</link>
            <description>Authors: Coe H, Michalak M
    ERp57 is a 58-kDa thiol oxidoreductase and a member of the protein disulfide isomerase (PDI)-like family. ERp57 is highly similar to other PDI family members in terms of amino acid sequence and structural/functional domain organization; however, it possesses some distinctive structural features that dictate its unique functions in the cell. This protein plays an important role in endoplasmic reticulum quality control of newly synthesized glycoproteins, is critical in major histocompatability complex (MHC) class I assembly and regulates gene expression. Studies on ERp57-deficient mice indicate that the protein is critical during embryonic development. The protein has been implicated in human pathologies including cancer and Alzheimer's disease.
    PMID: 20079...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186200</comments>
            <pubDate>Wed, 13 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186200</guid>        </item>
        <item>
            <title>Sepsis increases the expression and activity of the transcription factor forkhead box o 1 (foxo1) in skeletal muscle by a glucocorticoid-dependent mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=3186203&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20079455%26dopt%3DAbstract</link>
            <description>SEPSIS INCREASES THE EXPRESSION AND ACTIVITY OF THE TRANSCRIPTION FACTOR FORKHEAD BOX O 1 (FOXO1) IN SKELETAL MUSCLE BY A GLUCOCORTICOID-DEPENDENT MECHANISM.
    Int J Biochem Cell Biol. 2010 Jan 12;
    Authors: Smith IJ, Alamdari N, O'Neal P, Gonnella P, Aversa Z, Hasselgren PO
    Sepsis-induced muscle wasting has severe clinical consequences, including muscle weakness, need for prolonged ventilatory support and stay in the intensive care unit, and delayed ambulation with risk for pulmonary and thromboembolic complications. Understanding molecular mechanisms regulating loss of muscle mass in septic patients therefore has significant clinical implications. FOXO transcription factors have been implicated in muscle wasting, partly reflecting upregulation of the ubiquitin ligases atrogin-1 ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3186203</comments>
            <pubDate>Tue, 12 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3186203</guid>        </item>
        <item>
            <title>Mitochondrial Medicine for Neurodegenerative Diseases.</title>
            <link>http://www.medworm.com/index.php?rid=3172102&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20067840%26dopt%3DAbstract</link>
            <description>Authors: Du H, Yan SS
    Mitochondrial dysfunction has been reported in a wide array of neurological disorders ranging from neuromuscular to neurodegenerative diseases. Recent studies on neurodegenerative diseases have revealed that mitochondrial pathology is generally found in inherited or sporadic neurodegenerative diseases and is believed to involve in the pathophysiological process of these diseases. Commonly seen types of mitochondrial dysfunction in neurodegenerative diseases include excessive free radical generation, lowered ATP production, mitochondrial permeability transition, mitochondrial DNA lesions, perturbed mitochondrial traffic/dynamics and apoptosis. Mitochondrial medicine as an emerging therapeutic strategy targeted to mitochondrial dysfunction in neurodegenerative disea...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3172102</comments>
            <pubDate>Sat, 09 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3172102</guid>        </item>
        <item>
            <title>Nlrc4/Ipaf/CLAN/CARD12: more than a flagellin sensor.</title>
            <link>http://www.medworm.com/index.php?rid=3172101&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20067841%26dopt%3DAbstract</link>
            <description>Authors: Abdelaziz DH, Amr K, Amer AO
    Nlrc4 is a member of the Nod-like receptors (NLRs), a family of cytosolic receptors involved in sensing bacterial molecules. NLRs are a group of proteins containing spans of leucine-rich repeats that senses bacterial factors within the eukaryotic cytosol. The recognition of bacterial factors provokes the formation of the inflammasome complex which includes specific NLRs. The inflammasome is responsible for caspase-1 activation which leads to the cleavage and maturation of inflammatory cytokines such as IL-1beta and IL-18. Nlrc4 was considered to be a devoted flagellin sensor in eukaryotic cells. However, studies using a variety of pathogens such as Salmonella, Legionella, Shigella and Pseudomonas at high bacterial burdens revealed that Nlrc4 can me...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3172101</comments>
            <pubDate>Sat, 09 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3172101</guid>        </item>
        <item>
            <title>The cell biology of Hepatitis C Virus (HCV) lipid addiction: molecular mechanisms and its potential importance in the clinic.</title>
            <link>http://www.medworm.com/index.php?rid=3172100&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20067842%26dopt%3DAbstract</link>
            <description>Authors: Eric P, Philippe R, Jean-Christophe P
    Hepatitis C virus (HCV) is a major cause of chronic hepatitis associated with liver steatosis, commonly evolving to cirrhosis or hepatocellular carcinoma. The World Health Organisation (WHO) estimates that there are around 170 million chronic HCV carriers worldwide. The virus has a highly variable sequence, allowing definition of 7 genotypes with different geographical distributions. Both clinical outcome and response to antiviral therapy are strongly influenced by HCV genotype. Importantly, several recent papers have suggested that the lipid profile of infected patients is strongly indicative of the various clinical outcomes of HCV infection. Furthermore, viral molecular and cellular studies have shown a tight link between cellular lipid ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3172100</comments>
            <pubDate>Sat, 09 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3172100</guid>        </item>
        <item>
            <title>Reduced stability and enhanced surface hydrophobicity drive the binding of apo-aconitase with GroEL during chaperone assisted refolding.</title>
            <link>http://www.medworm.com/index.php?rid=3164228&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060926%26dopt%3DAbstract</link>
            <description>Authors: Gupta P, Mishra S, Chaudhuri TK
    Apo-aconitase, the Fe(4)S(4) cluster free form of TCA cycle enzyme aconitase, binds with GroEL and dissociates itself upon maturation through insertion of the cluster. It is not clearly established as to why apo-protein binds with GroEL. In order to explore the possibility, that stability is a factor responsible for the aggregation of apo-form at low ionic strengths and hence it associates with GroEL to avoid the unfavorable event, we carried out the unfolding studies with holo- and apo-aconitase. By probing the unfolding process through the changes in secondary structural element, exposed surface hydrophobicity, and the microenvironment around tryptophan residues, we were able to establish the relevant changes associated with the event. Apparen...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164228</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164228</guid>        </item>
        <item>
            <title>Exacerbation of tobacco smoke mediated apoptosis by resveratrol: an unexpected consequence of its antioxidant action.</title>
            <link>http://www.medworm.com/index.php?rid=3164227&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060927%26dopt%3DAbstract</link>
            <description>In conclusion, results from this study suggest that although resveratrol increased antioxidant and detoxification capacity, it increased rather than protected against cigarette smoke-induced apoptosis.
    PMID: 20060927 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164227</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164227</guid>        </item>
        <item>
            <title>The alternatively spliced murine Pregnane X Receptor isoform, mPXR(Delta171-211) exhibits a repressive action.</title>
            <link>http://www.medworm.com/index.php?rid=3164226&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060928%26dopt%3DAbstract</link>
            <description>Authors: Matic M, Corradin AP, Tsoli M, Clarke SJ, Polly P, Robertson GR
    The orphan nuclear receptor pregnane X receptor regulates enzymes and transport proteins involved in the detoxification and clearance of numerous endobiotic and xenobiotic compounds, including pharmaceutical agents. Multiple alternatively spliced pregnane X receptor isoforms have been identified which are significantly expressed in humans and mice (up to 30% of the total pregnane X receptor transcript), however, little is known about their biological action. We explored functional differences between the major mouse pregnane X receptor isoforms mPXR(431) and mPXR(Delta171-211) that lacks 41 amino acids adjacent to the ligand binding pocket. Transient transfection assays showed that mPXR(Delta171-211) reduced the b...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164226</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164226</guid>        </item>
        <item>
            <title>Negative feedback loop of BRCA1-BARD1 ubiquitin ligase on estrogen receptor alpha stability and activity antagonized by cancer-associated isoform of BARD1.</title>
            <link>http://www.medworm.com/index.php?rid=3164225&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060929%26dopt%3DAbstract</link>
            <description>We report that the Estrogen Receptor alpha is a target of the BRCA1-BARD1 ubiquitin ligase in vivo. BRCA1 and BARD1 are required for Estrogen Receptor alpha ubiquitination and degradation, and repression of either one leads to ERalpha accumulation, suggesting a feedback loop between BRCA1-BARD1 and Estrogen Receptor alpha, since BRCA1 and BARD1 are induced by Estrogen Receptor alpha. While the ubiquitin ligase activity maps to the N-terminal RING finger domains of BRCA1 and BARD1, we demonstrate that the BARD1 C-terminus is important for target recognition. Furthermore, a BARD1 isoform lacking the RING domain binds and stabilizes Estrogen Receptor alpha. Thus deficiencies of BRCA1 or BARD1 and/or upregulation of BARD1 isoforms lead to Estrogen Receptor alpha upregulation, providing a funct...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164225</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164225</guid>        </item>
        <item>
            <title>The fourth isoform of the adenine nucleotide translocator inhibits mitochondrial apoptosis in cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3164224&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060930%26dopt%3DAbstract</link>
            <description>Authors: Gallerne C, Touat Z, Chen ZX, Martel C, Mayola E, Dein OS, Buron N, Le Bras M, Jacotot E, Borgne-Sanchez A, Lemoine A, Lemaire C, Pervaiz S, Brenner C
    The adenine nucleotide translocator (ANT) is a mitochondrial bi-functional protein, which catalyzes the exchange of ADP and ATP between cytosol and mitochondria and participates in many models of mitochondrial apoptosis. The human adenine nucleotide translocator sub-family is composed of four isoforms, namely ANT1-4, encoded by four nuclear genes, whose expression is highly regulated. Previous studies have revealed that ANT1 and 3 induce mitochondrial apoptosis, whereas ANT2 is anti-apoptotic. However, the role of the recently identified isoform ANT4 in the apoptotic pathway has not yet been elucidated. Here, we investigated the...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164224</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164224</guid>        </item>
        <item>
            <title>The TAK1-TRAF6 signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3164223&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060931%26dopt%3DAbstract</link>
            <description>Authors: Landstr&amp;#xF6;m M
    Cellular responses to pathogens, growth factors, cytokines, extra- or intra-cellular stress, is a prerequisite for the cell to adapt to novel and potentially dangerous situations. If the changes in the extra- or intra-cellular milieu causes DNA-damage or revoke a signalling pathway utilized during morphogenesis, the epithelial cells might be forced to undergo programmed cell death (apoptosis) in the benefit for the whole organism or transform to a mesenchymal cell type (epithelial to mesenchymal transition; EMT), in respond to a specific stimuli. An overview is presented over the current knowledge for the key components in signal transduction in homeostasis, inflammation and cancer. A handful of transcription factors are crucial for the determination of the sp...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3164223</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3164223</guid>        </item>
        <item>
            <title>Molecules in Focus: Annexin A6-regulator of the EGFR/Ras signalling pathway and cholesterol homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=3137058&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044025%26dopt%3DAbstract</link>
            <description>Authors: Grewal T, Koese M, Rentero C, Enrich C
    Annexin A6 (AnxA6) belongs to the highly conserved annexin protein family. Like other annexins, the function of AnxA6 is linked to its ability to bind phospholipids in a Ca(2+)-dependent manner, thereby interacting with cellular membranes in a dynamic, reversible and regulated fashion. Upon cell activation, AnxA6 is recruited to the plasma membrane, endosomes and caveolae/membrane rafts to interact with signalling proteins, the endocytic machinery and actin cytoskeleton to inhibit epidermal growth factor receptor and Ras signalling. In addition, AnxA6 associates with late endosomes to regulate cholesterol export leading to reduced cytoplasmic phospholipase A2 activity and caveolae formation. Accordingly, AnxA6 may function as an organizer...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3137058</comments>
            <pubDate>Mon, 28 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3137058</guid>        </item>
        <item>
            <title>Adiponectin-it's all about the modifications.</title>
            <link>http://www.medworm.com/index.php?rid=3137057&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20044026%26dopt%3DAbstract</link>
            <description>Authors: Simpson F, Whitehead JP
    Adiponectin is an adipokine (adipocyte-derived hormone) with multiple salutary effects. It is secreted into the circulation as low molecular weight (LMW) and high molecular weight (HMW) multimers with the latter being more metabolically active. Extensive post-translational modifications (PTMs) are required for efficient adiponectin multimerisation and secretion. Recent studies have identified novel PTMs that contribute to the efficacy of adiponectin production and clearance. Thiol-mediated retention of adiponectin occurs during transit through the ER, via direct interactions with chaperones including ERp44 and DsbA-L, and facilitates multimerisation and secretion. Interestingly, this appears to be in direct competition with adiponectin succination. Adip...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3137057</comments>
            <pubDate>Mon, 28 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3137057</guid>        </item>
        <item>
            <title>E-i-C Editorial: Structure and function of the SOX transcription factors.</title>
            <link>http://www.medworm.com/index.php?rid=3129934&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20036754%26dopt%3DAbstract</link>
            <description>Authors: Kargul J, Laurent GJ
    
    PMID: 20036754 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3129934</comments>
            <pubDate>Thu, 24 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3129934</guid>        </item>
        <item>
            <title>Role of microRNAs in ovarian cancer pathogenesis and potential clinical implications.</title>
            <link>http://www.medworm.com/index.php?rid=3129936&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20035894%26dopt%3DAbstract</link>
            <description>Authors: Mezzanzanica D, Bagnoli M, De Cecco L, Valeri B, Canevari S
    Despite important improvements over the past two decades, the overall cure rate of epithelial ovarian cancer (EOC) remains only approximately 30%. Although much has been learned about the proteins and pathways involved in early events of malignant transformation and drug resistance, a major challenge still remaining is the identification of markers for early diagnosis and prediction of response to chemotherapy. Recently, it has become clear that alterations in the expression of microRNAs (miRNA) contribute to the pathogenesis and progression of several human malignancies. In this review we discuss current data concerning the accumulating evidence of the role of miRNAs in EOC pathogenesis and tumor characterization; th...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3129936</comments>
            <pubDate>Tue, 22 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3129936</guid>        </item>
        <item>
            <title>NFATc1: Functions in Osteoclasts.</title>
            <link>http://www.medworm.com/index.php?rid=3129935&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20035895%26dopt%3DAbstract</link>
            <description>Authors: Zhao Q, Wang X, Liu Y, He A, Jia R
    NFATc1 is an important transcription factor which is critical for lineage selection in T-cell differentiation, cardiac valve morphogenesis, lymphatic endothelial development, osteoblast differentiation and osteoclastogenesis. Especially, it is a master regulator of RANKL-induced osteoclast differentiation and plays a pivotal role in osteoclast fusion and osteoclast activation via up-regulation of various genes responsible for osteoclast adhesion, migration, acidication, degradation of inorganic and organic bone matrix. In the present review,some of the known features of NFATc1 such as structure, function and its roles in physiological or pathophysiological processes are highlighted.
    PMID: 20035895 [PubMed - as supplied by publisher] (Sour...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3129935</comments>
            <pubDate>Tue, 22 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3129935</guid>        </item>
        <item>
            <title>Human Circulating Fibrocytes Have The Capacity To Differentiate Osteoblasts And Chondrocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3122537&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20034590%26dopt%3DAbstract</link>
            <description>In this study, we found that fibrocytes differentiated into osteoblast-like cells when cultured in osteogenic media in a manner similar to osteoblast precursor cells. Under these conditions, fibrocytes and osteoblast precursor cells displayed increased calcium deposition, and increased expression of specific osteogenic genes. In addition, dephosphorylation of cAMP-responsive element binding protein was associated with the increased ratio of Receptor activator of the NF-kappaB Ligand/osteoprotegerin gene expression and enhanced gene expression of osterix in these cells under these conditions. Both events are important in promoting osteogenesis. In contrast, fibrocytes and mesenchymal stem cells cultured in chondrogenic media in the presence of transforming growth factor-beta3 were found to ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3122537</comments>
            <pubDate>Mon, 21 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3122537</guid>        </item>
        <item>
            <title>Transporters, channels, or simple diffusion? Dogmas, atypical roles and complexity in transport systems.</title>
            <link>http://www.medworm.com/index.php?rid=3119406&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20026419%26dopt%3DAbstract</link>
            <description>Authors: Conde A, Diallinas G, Chaumont F, Chaves M, Ger&amp;#xF3;s H
    The recent breakthrough discoveries of transport systems assigned with atypical functions provide evidence for complexity in membrane transport biochemistry. Some channels are far from being simple pores creating hydrophilic passages for solutes and can, unexpectedly, act as enzymes, or mediate high-affinity uptake, and some transporters are surprisingly able to function as sensors, channels or even enzymes. Furthermore, numerous transport studies have demonstrated complex multiphasic uptake kinetics for organic and mineral nutrients. The biphasic kinetics of glucose uptake in Saccharomyces cerevisiae, a result of several genetically distinct uptake systems operating simultaneously, is a classical example that is a subje...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119406</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119406</guid>        </item>
        <item>
            <title>The Resolution of Inflammation: Anti-inflammatory roles for NF-kappaB.</title>
            <link>http://www.medworm.com/index.php?rid=3119405&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20026420%26dopt%3DAbstract</link>
            <description>Authors: Lawrence T, Fong C
    Inflammation is a salutary response to insult or injury that normally resolves with no detriment to the host. While the mechanisms and mediators that regulate the onset of inflammation have been well characterized we still know relatively little about the endogenous mechanisms that terminate the inflammatory response [1]. Nuclear factor (NF)-kappaB is a generic term for a family of ubiquitous transcription factors with diverse physiological functions [2,3]. NF-kappaB transcription factors are formed by dimerisation of Rel proteins; RelA (p65), c-Rel, RelB, p50, p52. Various hetero or homodimers of Rel proteins can be formed in a tissue and stimulus specific manner, genetic evidence suggests these transcription factors have a critical role in cell survival an...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119405</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119405</guid>        </item>
        <item>
            <title>The complexity of the complicity of mast cells in cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3119404&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20026421%26dopt%3DAbstract</link>
            <description>Authors: Nechushtan H
    Mast cells are evolutionarly ancient cells of the immune cells which can secrete a variety of effector molecules. Animal and pathologic studies suggest that mast cells may promote tumor growth in some cancer types but may act in an opposite manner in others. In several mouse models a critical role of mast cells for tumor promotion was demonstrated. In humans mast cells are dependent upon the tyrosine kinase receptor c-Kit. This receptor is inhibited by many of the new anti-cancer tyrosine kinase inhibitors including Pazopanib, Imatinib and Masitinib. These drugs probably ablate some tumor mast cells, in addition to their other known anti tumor effects. Understanding the complex roles of mast cells in cancer should aid in understanding mechanisms of current tyrosin...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119404</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119404</guid>        </item>
        <item>
            <title>MicroRNAs: potential biomarkers for cancer diagnosis, prognosis and targets for therapy.</title>
            <link>http://www.medworm.com/index.php?rid=3119403&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20026422%26dopt%3DAbstract</link>
            <description>Authors: Cho WC
    MicroRNAs have a revolutionary impact on cancer research over recent years. They emerge as important players in tumorigenesis, leading to a paradigm shift in oncology. The widespread and comprehensive use of microRNA microarrays has enabled the identification of a number of microRNAs as potential biomarkers for cancer. It is encouraging to report that microRNAs have remarkable stability in both formalin-fixed tissue and blood. Many microRNAs have been identified to act as oncogenes, tumor suppressors, or even modulators of cancer stem cells and metastasis. Some studies not only reported the identified microRNA biomarkers, but also deciphered their target genes and the underlying mechanisms. The rapid discovery of many microRNA targets and their relevant pathways has con...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119403</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119403</guid>        </item>
        <item>
            <title>Eicosanoids and the endogenous control of acute inflammatory resolution.</title>
            <link>http://www.medworm.com/index.php?rid=3119402&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20026423%26dopt%3DAbstract</link>
            <description>Authors: Gilroy DW
    Inflammation is a formidable ally in the constant battle against infection, cancer and tissue injury. It's a primordial response that protects against injury and restores damaged tissue to its normal physiological functioning. In fact, our wellbeing and survival depends upon its efficiency and carefully-balanced control. In general, the innate inflammatory response initiates within minutes and, if all is well, resolves within hours. In contrast, chronic inflammation persists for weeks, months or even years. Here, we are going to discuss the key endogenous checkpoints necessary for mounting an effective yet limited inflammatory response and the crucial biochemical pathways necessary to prevent its persistence. In this setting, the biochemical synthesis of key pro-reso...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119402</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119402</guid>        </item>
        <item>
            <title>Scavenger receptors are associated with cellular interactions of S100A12 in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3119408&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20025991%26dopt%3DAbstract</link>
            <description>We report a novel methodology using recombinant human S100 proteins radiolabelled with fluorine-18, particularly, (18)F-S100A12, in receptor binding studies and cellular association studies in vitro, and in dynamic small animal positron emission tomography (PET) studies in rats in vivo. Association to both human aortic endothelial cells and macrophages revealed specific binding of (18)F-S100A12 to RAGE, but, furthermore, provides evidence for interaction of (18)F-S100A12 to various scavenger receptors (SR). PET data showed temporary association of (18)F-S100A12 with tissues overexpressing RAGE (e.g., lung), and, moreover, accumulation of (18)F-S100A12 in tissues enriched in cells overexpressing SR (e.g., liver and spleen). Blockade of overall SR interaction by maleylated BSA (malBSA) clear...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119408</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119408</guid>        </item>
        <item>
            <title>Medicine in Focus: Lipolysis in Adipocytes.</title>
            <link>http://www.medworm.com/index.php?rid=3119407&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20025992%26dopt%3DAbstract</link>
            <description>Authors: Ahmadian M, Wang Y, Sul HS
    Lipolysis in adipocytes, the hydrolysis of triacylglycerol (TAG) to release fatty acids (FAs) and glycerol for use by other organs, is a unique function of white adipose tissue. Lipolysis in adipocytes occurs at the surface of cytosolic lipid droplets, which have recently gained much attention as dynamic organelles integral to lipid metabolism. Desnutrin/ATGL is now established as a bona fide TAG hydrolase and mutations in human desnutrin/ATGL/PNPLA2, as well as in its activator, comparative gene identification 58, are associated with Neutral Lipid Storage disease. Furthermore, recent identification of AdPLA as the major adipose phospholipase A(2), has led to the discovery of a dominant autocrine/paracrine regulation of lipolysis through PGE(2). Here...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3119407</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3119407</guid>        </item>
        <item>
            <title>The co-chaperone BAG3 interacts with the cytosolic chaperonin CCT: new hints for actin folding.</title>
            <link>http://www.medworm.com/index.php?rid=3105391&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20018251%26dopt%3DAbstract</link>
            <description>Authors: Fontanella B, Birolo L, Infusini G, Cirulli C, Marzullo L, Pucci P, Turco MC, Tosco A
    It has been recently hypothesized that BAG3 protein, a co-chaperone of Hsp70/Hsc70, is involved in the regulation of several cell processes, such as apoptosis, autophagy and cell motility. Following the identification of Hsc70/Hsp70, further BAG3 molecular partners such as PLC-gamma and HspB8 were likewise identified, thus contributing to the characterization of the mechanisms and the biological roles carried out by this versatile protein. By using a His-tagged BAG3 protein as bait, we fished out and identified the cytosolic chaperonin CCT, a new unreported BAG3 partner. The interaction between BAG3 and CCT was confirmed and characterized by co-immunoprecipitation experiments and surface plas...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105391</comments>
            <pubDate>Mon, 14 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105391</guid>        </item>
        <item>
            <title>Adult human brain cell culture for neuroscience research.</title>
            <link>http://www.medworm.com/index.php?rid=3105397&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20004737%26dopt%3DAbstract</link>
            <description>Authors: Gibbons HM, Dragunow M
    Studies of the brain have progressed enormously through the use of in vivo and in vitro non-human models. However, it is unlikely such studies alone will unravel the complexities of the human brain and so far no neuroprotective treatment developed in animals has worked in humans. In this review we discuss the use of adult human brain cell culture methods in brain research to unravel the biology of the normal and diseased human brain. The advantages of using adult human brain cells as tools to study human brain function from both historical and future perspectives are discussed. In particular, studies using dissociated cultures of adult human microglia, astrocytes, oligodendrocytes and neurons are described and the applications of these types of study are...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105397</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105397</guid>        </item>
        <item>
            <title>Lymphoid enhancer factor-1 mediates loading of Pax3 to a promoter harbouring lymphoid enhancer factor-1 binding sites resulting in enhancement of transcription.</title>
            <link>http://www.medworm.com/index.php?rid=3105393&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20006729%26dopt%3DAbstract</link>
            <description>We describe here a novel mode of Pax3-dependent regulation of transcription that is mediated through DNA-independent binding to Lef1. Specifically, we demonstrate that Pax3 binds to Lef1, determined in binding assays and co-immunoprecipitation of endogenous Pax3 and Lef1. Binding assays employing deletion mutants of Pax3 and Lef1 determined that association was mediated through the homeodomain of Pax3 and the first half of the Lef1 DNA-binding domain. The significance of this association was demonstrated in transcriptional assays using a luciferase reporter gene downstream of a model promoter harbouring Lef1 DNA-binding consensus sites. Pax3 augmented Lef1-dependent transactivation from this promoter. This increase in transcriptional activity occurred in the absence and presence of added b...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105393</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105393</guid>        </item>
        <item>
            <title>Neuropathy target esterase: An essential enzyme for neural development and axonal maintenance.</title>
            <link>http://www.medworm.com/index.php?rid=3105392&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20006730%26dopt%3DAbstract</link>
            <description>Authors: Chang PA, Wu YJ
    Neuropathy target esterase (NTE) is an endoplasmic reticulum-anchored protein conserved across species. The N-terminal regulatory region of NTE contains three cyclic nucleotide binding domains while the C-terminal catalytic domain has a patatin domain. The NTE gene is expressed in mouse early at embryonic day 7 and its expression is maintained throughout embryonic development. NTE protein is mainly distributed in the nervous system with a pattern that is more restricted to large neurons in older animals. NTE regulates phospholipid metabolism and is known to be a phospholipase B. Knockout of NTE is embryonic lethal in mice, indicating that NTE is essential for embryonic survival. Neuronal specific NTE knock-outs survive to adulthood, but show vacuolation and neu...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105392</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105392</guid>        </item>
        <item>
            <title>The early history of the Sox genes.</title>
            <link>http://www.medworm.com/index.php?rid=3105396&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20005971%26dopt%3DAbstract</link>
            <description>Authors: Lovell-Badge R
    
    PMID: 20005971 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105396</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105396</guid>        </item>
        <item>
            <title>SRY: a transcriptional activator of mammalian testis determination.</title>
            <link>http://www.medworm.com/index.php?rid=3105395&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20005972%26dopt%3DAbstract</link>
            <description>Authors: Sekido R
    Sry (sex-determining region Y) is the sex-determining gene on the mammalian Y chromosome, which encodes a transcription factor containing a DNA-binding domain characteristic of some high mobility group proteins (HMG box). It is the founder member of the Sox (Sry-related HMG box) gene family and is therefore classified in the SOX A group. In mice, the transient expression of Sry between 10.5 and 12.5 dpc triggers the differentiation of Sertoli cells from the supporting cell precursor lineage, which would otherwise give rise to granulosa cells in ovaries. However, little was known about the target genes of SRY and molecular mechanisms how SRY leads to testis development. Recent work has provided evidence that SRY binds directly to a testis-specific enhancer of Sox9 (TES...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105395</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105395</guid>        </item>
        <item>
            <title>Proteomics Identifies Multipotent and Low Oncogenic Risk Stem Cells of the Spleen.</title>
            <link>http://www.medworm.com/index.php?rid=3105394&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20005973%26dopt%3DAbstract</link>
            <description>Authors: Dieguez-Acu&amp;#xF1;a F, Kodama S, Okubo Y, Paz AC, Gygi SP, Faustman DL
    The adult spleen harbors a population of naturally occurring multipotent stem cells of non-lymphoid lineage (CD45-). In animal models, these splenic stem cells can directly or indirectly contribute to regeneration of bone, inner ear, cranial nerves, islets, hearts and salivary glands. Here we characterize the CD45- stem cell proteome to determine its potential broader multipotency versus its protection from malignant transformation. Using state-of-the-art proteomics and in vivo testing, we performed functional analyses of unique proteins of CD45- (non-lymphoid) splenic stem cells, as compared with CD45+ (lymphoid) cells. CD45- stem cell-specific proteins were identical to those in iPS, including OCT3/4, SOX2...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105394</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105394</guid>        </item>
        <item>
            <title>Twenty Sox, twenty years.</title>
            <link>http://www.medworm.com/index.php?rid=3105398&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20004736%26dopt%3DAbstract</link>
            <description>Authors: Harley V, Lefebvre V
    
    PMID: 20004736 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3105398</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3105398</guid>        </item>
        <item>
            <title>MicroRNAs: Potential Regulators Involved in Human Anencephaly.</title>
            <link>http://www.medworm.com/index.php?rid=3065327&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19962448%26dopt%3DAbstract</link>
            <description>In this study, we show the presence of a specific miRNA expression profile from tissues of fetuses with anencephaly, one of the most severe forms of NTDs. Furthermore, we map the target genes of these miRNAs in the human genome. In comparison to healthy human fetal brain tissues, tissues from fetuses with anencephaly exhibited 97 down-regulated and 116 up-regulated miRNAs. The microarray findings were extended using real-time qRT-PCR for nine miRNAs. Specifically, of these validated miRNAs, miR-126, miR-198, and miR-451 were up-regulated, while miR-9, miR-212, miR-124, miR-138, and miR-103/107 were down-regulated in the tissues of fetuses with anencephaly. A bioinformatic analysis showed 881 potential target genes that are regulated by the validated miRNAs. Seventy-nine of these potential ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3065327</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3065327</guid>        </item>
        <item>
            <title>Histone acetyltransferases interact with and acetylate p70 ribosomal S6 kinases in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3065328&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19961954%26dopt%3DAbstract</link>
            <description>Authors: Fenton TR, Gwalter J, Ericsson J, Gout IT
    The 70kDa ribosomal protein S6 kinases (S6K1 and S6K2) play important roles in the regulation of protein synthesis, cell growth and survival. S6Ks are activated in response to mitogen stimulation and nutrient sufficiency by the phosphorylation of conserved serine and threonine residues. Here we show for the first time, that in addition to phosphorylation, S6Ks are also targeted by lysine acetylation. Following mitogen stimulation, S6Ks interact with the p300 and p300/CBP associated factor (PCAF) acetyltransferases. S6Ks can be acetylated by p300 and PCAF in vitro and S6K acetylation is detected in cells expressing p300. Furthermore, it appears that the acetylation sites targeted by p300 lie within the divergent C-terminal regulatory do...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3065328</comments>
            <pubDate>Tue, 01 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3065328</guid>        </item>
        <item>
            <title>Neurotensin receptor-2 and -3 are crucial for the anti-apoptotic effect of neurotensin on pancreatic beta-TC3 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2972177&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19891061%26dopt%3DAbstract</link>
            <description>Authors: B&amp;#xE9;raud-Dufour S, Coppola T, Massa F, Mazella J
    The neuropeptide neurotensin (NT) has been recently shown to protect pancreatic beta cells from toxic agents-induced apoptosis through interaction with the NT receptor-2 (NTSR2) and activation of the phosphatidylinositol-3 kinase pathway. However, expression of the NT receptor-3/sortilin (NTSR3) in the mouse pancreatic beta cell line -TC3 led us to investigate its possible functional role in these cells. By using siRNA, immunoprecipitation, co-localization and caspase-3 assays,we provide evidence for a functional endogenous interaction between NTSR2 and NTSR3. Expression of both receptors is necessary for the protective action of NT on staurosporine-induced caspase-3 activity in -TC3 cells. Moreover, NTSR2 and NTSR3 co-immuno...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2972177</comments>
            <pubDate>Sun, 08 Nov 2009 23:34:05 +0100</pubDate>
            <guid isPermaLink="false">2972177</guid>        </item>
        <item>
            <title>Hepatic myofibroblasts: a heterogeneous population of multifunctional cells in liver fibrogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2847073&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19782946%26dopt%3DAbstract</link>
            <description>Authors: Novo E, di Bonzo LV, Cannito S, Colombatto S, Parola M
    Hepatic myofibroblasts constitute a heterogeneous population of highly proliferative, pro-fibrogenic, pro-inflammatory, pro-angiogenic and contractile cells that sustain liver fibrogenesis and then fibrotic progression of chronic liver diseases of different aetiology to the common advanced-stage of cirrhosis. These alpha-smooth muscle actin-positive myofibroblast-like cells, according to current literature, mainly originate by a process of activation and trans-differentiation that involves either hepatic stellate cells or fibroblasts of portal areas. Hepatic myofibroblasts can also originate from bone marrow-derived cells, including mesenchymal stem cells or circulating fibrocytes able to engraft chronically injured liver,...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847073</comments>
            <pubDate>Thu, 01 Oct 2009 00:22:15 +0100</pubDate>
            <guid isPermaLink="false">2847073</guid>        </item>
        <item>
            <title>O-GlcNAc cycling: implications for neurodegenerative disorders.</title>
            <link>http://www.medworm.com/index.php?rid=2847072&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19782947%26dopt%3DAbstract</link>
            <description>Authors: Lazarus BD, Love DC, Hanover JA
    The dynamic post-translational modification of proteins by O-linked N-acetylglucosamine (O-GlcNAc), termed O-GlcNAcylation, is an important mechanism for modulating cellular signaling pathways. O-GlcNAcylation impacts transcription, translation, organelle trafficking, proteasomal degradation and apoptosis. O-GlcNAcylation has been implicated in the etiology of several human diseases including type-2 diabetes and neurodegeneration. This review describes the pair of enzymes responsible for the cycling of this post-translational modification: O-GlcNAc transferase (OGT) and beta-N-acetylglucosaminidase (OGA), with a focus on the function of their structural domains. We will also highlight the important processes and substrates regulated by these enz...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847072</comments>
            <pubDate>Thu, 01 Oct 2009 00:22:12 +0100</pubDate>
            <guid isPermaLink="false">2847072</guid>        </item>
        <item>
            <title>Endothelial CD146 is required for in vitro tumor-induced angiogenesis: the role of a disulfide bond in signaling and dimerization.</title>
            <link>http://www.medworm.com/index.php?rid=2847071&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19782948%26dopt%3DAbstract</link>
            <description>Authors: Zheng C, Qiu Y, Zeng Q, Zhang Y, Lu D, Yang D, Feng J, Yan X
    Tumor angiogenesis, induced by tumor-secreted pro-angiogenic factors, is an essential process for cancer development and metastasis. CD146 is identified as an endothelial cell adhesion molecule and implicated in blood vessel formation, however, its exact role in angiogenesis, particularly tumor angiogenesis, and its potential function of mediating downstream signaling are still unclear. In present study, we evidenced that silencing endogenous endothelial CD146 by RNAi significantly impaired hepatocarcinoma cell secretions-promoted tubular morphogenesis and -enhanced motility of endothelial cells. Biochemical studies revealed that CD146 was required for the activation of p38/IKK/NF kappaB signaling cascade and up-regu...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847071</comments>
            <pubDate>Thu, 01 Oct 2009 00:22:09 +0100</pubDate>
            <guid isPermaLink="false">2847071</guid>        </item>
        <item>
            <title>Downregulation of protein tyrosine phosphatase PTP-BL represses adipogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2847070&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19782949%26dopt%3DAbstract</link>
            <description>Authors: Glondu-Lassis M, Dromard M, Chavey C, Puech C, Fajas L, Hendriks W, Freiss G
    The insulin/insulin-like growth factor 1 (IGF-1) signaling pathway is a major regulator of adipose tissue growth and differentiation. We recently demonstrated that human protein tyrosine phosphatase (PTP) L1, a large cytoplasmic phosphatase also known as PTP-BAS/PTPN13/PTP-1E, is a negative regulator of IGF-1R/IRS-1/Akt pathway in breast cancer cells. This triggered us to investigate the potential role of PTPL1 in adipogenesis. To evaluate the implication of PTP-BL, the mouse orthologue of PTPL1, in adipose tissue biology, we analyzed PTP-BL mRNA expression in adipose tissue in vivo and during proliferation and differentiation of 3T3-L1 pre-adipocytes. To elucidate the role of PTP-BL and of its cataly...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847070</comments>
            <pubDate>Thu, 01 Oct 2009 00:22:07 +0100</pubDate>
            <guid isPermaLink="false">2847070</guid>        </item>
        <item>
            <title>The role of phosphorylated glucocorticoid receptor in mitochondrial functions and apoptotic signalling in brain tissue of stressed Wistar rats.</title>
            <link>http://www.medworm.com/index.php?rid=2847069&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19782950%26dopt%3DAbstract</link>
            <description>Authors: Adzic M, Djordjevic A, Demonacos C, Krstic-Demonacos M, Radojcic MB
    Mitochondrial dysfunction is increasingly recognized as a key component in compromised neuroendocrine stress response and, among other etiological causes, it may also involve action of glucocorticoid hormones. In the current study we followed glucocorticoid receptor and identified its mitochondrial phosphoisophorms in hippocampus and prefrontal brain cortex of Wistar male rats subjected to acute, chronic and combined neuroendocrine stresses. In both brain structures chronic social isolation caused marked increase in mitochondrial glucocorticoid receptor that was preferentially phosphorylated at serine 232 compared to serine 246 or serine 171. This increase corresponded with the decreased expression of mitochon...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2847069</comments>
            <pubDate>Thu, 01 Oct 2009 00:22:04 +0100</pubDate>
            <guid isPermaLink="false">2847069</guid>        </item>
        <item>
            <title>Structural and functional organization of the mitochondrial respiratory chain: a dynamic super-assembly.</title>
            <link>http://www.medworm.com/index.php?rid=2741971&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19711505%26dopt%3DAbstract</link>
            <description>Authors: Lenaz G, Genova ML
    The structural organization of the mitochondrial oxidative phosphorylation (OXPHOS) system has received large attention in the past and most investigations led to the conclusion that the respiratory enzymatic complexes are randomly dispersed in the lipid bilayer of the inner membrane and functionally connected by fast diffusion of smaller redox components, Coenzyme Q and cytochrome c. More recent investigations by native gel electrophoresis, however, have shown the existence of supramolecular associations of the respiratory complexes, confirmed by electron microscopy analysis and single particle image processing. Flux control analysis has demonstrated that Complexes I and III in mammalian mitochondria and Complexes I, III, and IV in plant mitochondria kineti...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2741971</comments>
            <pubDate>Fri, 28 Aug 2009 22:34:05 +0100</pubDate>
            <guid isPermaLink="false">2741971</guid>        </item>
        <item>
            <title>Mitochondrial dynamics in human NADH:ubiquinone oxidoreductase deficiency.</title>
            <link>http://www.medworm.com/index.php?rid=2734963&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703648%26dopt%3DAbstract</link>
            <description>Authors: Willems PH, Smeitink JA, Koopman WJ
    Mitochondrial NADH:ubiquinone oxidoreductase or complex I (CI) is a frequently affected enzyme in cases of mitochondrial disorders. However, the cytopathological mechanism of the associated pediatric syndromes is poorly understood. Evidence in the literature suggests a connection between mitochondrial metabolism and morphology. Previous quantitative analysis of mitochondrial structure in cultured fibroblasts of 14 patients revealed that mitochondria were fragmented and/or less branched in patients with severe CI deficiency. These patient cells also displayed greatly increased levels of reactive oxygen species (ROS) and marked aberrations in mitochondrial and cellular Ca(2+)/ATP handling upon hormone stimulation. Here, we discuss the interrel...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734963</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:41 +0100</pubDate>
            <guid isPermaLink="false">2734963</guid>        </item>
        <item>
            <title>Mitochondrial F1F0-ATP synthase and organellar internal architecture.</title>
            <link>http://www.medworm.com/index.php?rid=2734962&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703649%26dopt%3DAbstract</link>
            <description>Authors: Velours J, Dautant A, Salin B, Sagot I, Br&amp;#xE8;thes D
    The mitochondrial F(1)F(0)-ATP synthase adopts supramolecular structures. The interaction domains between monomers involve components belonging to the F(0) domains. In Saccharomyces cerevisiae, alteration of these components destabilizes the oligomeric structures, leading concomitantly to the appearance of monomeric species of ATP synthase and anomalous mitochondrial morphologies in the form of onion-like structures. The mitochondrial ultrastructure at the cristae level is thus modified. Electron microscopy on cross-sections of wild type mitochondria display many short cristae with narrowed intra-cristae space, whereas yeast mutants defected in supramolecular ATP synthases assembly present a low number of large lamellar cr...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734962</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:39 +0100</pubDate>
            <guid isPermaLink="false">2734962</guid>        </item>
        <item>
            <title>Mitochondrial reticulum network dynamics in relation to oxidative stress, redox regulation, and hypoxia.</title>
            <link>http://www.medworm.com/index.php?rid=2734961&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703650%26dopt%3DAbstract</link>
            <description>Authors: Jezek P, Plecit&amp;#xE1;-Hlavat&amp;#xE1; L
    A single mitochondrial network in the cell undergoes constant fission and fusion primarily depending on the local GTP gradients and the mitochondrial energetics. Here we overview the main properties and regulation of pro-fusion and pro-fission mitodynamins, i.e. dynamins-related GTPases responsible for mitochondrial shape-forming, such as pro-fusion mitofusins MFN1, MFN2, and the inner membrane-residing long OPA1 isoforms, and pro-fission mitodynamins FIS1, MFF, and DRP1 multimers required for scission. Notably, the OPA1 cleavage into non-functional short isoforms at a diminished ATP level (collapsed membrane potential) and the DRP1 recruitment upon phosphorylation by various kinases are overviewed. Possible responses of mitodynamins to the...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734961</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:36 +0100</pubDate>
            <guid isPermaLink="false">2734961</guid>        </item>
        <item>
            <title>Interactions between the endoplasmic reticulum, mitochondria, plasma membrane and other subcellular organelles.</title>
            <link>http://www.medworm.com/index.php?rid=2734960&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703651%26dopt%3DAbstract</link>
            <description>Authors: Lebiedzinska M, Szabadkai G, Jones AW, Duszynski J, Wieckowski MR
    Several recent works show structurally and functionally dynamic contacts between mitochondria, the plasma membrane, the endoplasmic reticulum, and other subcellular organelles. Many cellular processes require proper cooperation between the plasma membrane, the nucleus and subcellular vesicular/tubular networks such as mitochondria and the endoplasmic reticulum. It has been suggested that such contacts are crucial for the synthesis and intracellular transport of phospholipids as well as for intracellular Ca(2+) homeostasis, controlling fundamental processes like motility and contraction, secretion, cell growth, proliferation and apoptosis. Close contacts between smooth sub-domains of the endoplasmic reticulum and...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734960</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:34 +0100</pubDate>
            <guid isPermaLink="false">2734960</guid>        </item>
        <item>
            <title>Importance of lipid metabolism for intracellular and mitochondrial membrane fusion/fission processes.</title>
            <link>http://www.medworm.com/index.php?rid=2734959&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703652%26dopt%3DAbstract</link>
            <description>Authors: Furt F, Moreau P
    Mitochondria move along cytoskeletal tracks, fuse and divide. These dynamic features have been shown to be critical for several mitochondrial functions in cell viability and cell death. After a rapid recall of the proteic machineries that are known to be involved, the review will focus on lipids, other key molecular actors of membrane dynamics. A summary of the current knowledge on lipids and their implication in various cellular membrane fusion/fission processes will be first presented. The review will then report what has been discovered or can be expected on the role of the different families of lipids in mitochondrial membrane fusion and fission processes.
    PMID: 19703652 [PubMed - in process] (Source: The International Journal of Biochemistry and Cell ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734959</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:32 +0100</pubDate>
            <guid isPermaLink="false">2734959</guid>        </item>
        <item>
            <title>Role of mitochondrial dynamics proteins in the pathophysiology of obesity and type 2 diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=2734958&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703653%26dopt%3DAbstract</link>
            <description>Authors: Zorzano A, Liesa M, Palac&amp;#xED;n M
    Mitochondrial dysfunction has been reported in skeletal muscle of obese subjects and of type 2 diabetic patients. Reduced mitochondrial mass and defective activity have been proposed to explain this dysfunction. Alterations in mitochondrial function may be crucial to explain the metabolic changes and insulin resistance that characterize both obesity and type 2 diabetes. Consequently, the identification of the primary mechanisms involved is of great relevance. Mitochondrial dynamics refers to the movement of mitochondria along the cytoskeleton and also to the regulation of mitochondrial morphology and distribution, which depend on fusion and fission events. In recent years, some of the proteins that participate in mitochondrial fusion and fiss...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734958</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:29 +0100</pubDate>
            <guid isPermaLink="false">2734958</guid>        </item>
        <item>
            <title>Mitochondrial DNA nucleoids determine mitochondrial genetics and dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=2734957&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703654%26dopt%3DAbstract</link>
            <description>Authors: Gilkerson RW
    Mitochondrial DNA plays a crucial role in cellular homeostasis; however, the molecular mechanisms underlying mitochondrial DNA inheritance and propagation are only beginning to be understood. To ensure the distribution and propagation of the mitochondrial genome, mitochondrial DNA is packaged into macromolecular assemblies called nucleoids, composed of one or more copies of mitochondrial DNA and associated proteins. We review current research on the mitochondrial nucleoid, including nucleoid-associated proteins, nucleoid dynamics within the cell, potential mechanisms to ensure proper distribution of nucleoids, and the impact of nucleoid organization on mitochondrial dysfunction. The nucleoid is the molecular organizing unit of mitochondrial genetics, and is the si...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734957</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:27 +0100</pubDate>
            <guid isPermaLink="false">2734957</guid>        </item>
        <item>
            <title>The cell-type specificity of mitochondrial dynamics.</title>
            <link>http://www.medworm.com/index.php?rid=2734956&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703655%26dopt%3DAbstract</link>
            <description>Authors: Kuznetsov AV, Hermann M, Saks V, Hengster P, Margreiter R
    Recent advances in mitochondrial imaging have revealed that in many cells mitochondria can be highly dynamic. They can undergo fission/fusion processes modulated by various mitochondria-associated proteins and also by conformational transitions in the inner mitochondrial membrane. Moreover, precise mitochondrial distribution can be achieved by their movement along the cytoskeleton, recruiting various connector and motor proteins. Such movement is evident in various cell types ranging from yeast to mammalian cells and serves to direct mitochondria to cellular regions of high ATP demand or to transport mitochondria destined for elimination. Existing data also demonstrate that many aspects of mitochondrial dynamics, morpho...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734956</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:25 +0100</pubDate>
            <guid isPermaLink="false">2734956</guid>        </item>
        <item>
            <title>From mitochondrial dynamics to arrhythmias.</title>
            <link>http://www.medworm.com/index.php?rid=2734955&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703656%26dopt%3DAbstract</link>
            <description>Authors: Aon MA, Cortassa S, Akar FG, Brown DA, Zhou L, O'Rourke B
    The reactive oxygen species (ROS)-dependent mitochondrial oscillator described in cardiac cells exhibits at least two modes of function under physiological conditions or in response to metabolic and oxidative stress. Both modes depend upon network behavior of mitochondria. Under physiological conditions cardiac mitochondria behave as a network of coupled oscillators with a broad range of frequencies. ROS weakly couples mitochondria under normal conditions but becomes a strong coupling messenger when, under oxidative stress, the mitochondrial network attains criticality. Mitochondrial criticality is achieved when a threshold of ROS is overcome and a certain density of mitochondria forms a cluster that spans the whole cel...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734955</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:22 +0100</pubDate>
            <guid isPermaLink="false">2734955</guid>        </item>
        <item>
            <title>Mitochondria in cardiomyocyte Ca2+ signaling.</title>
            <link>http://www.medworm.com/index.php?rid=2734954&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703657%26dopt%3DAbstract</link>
            <description>Authors: Lukyanenko V, Chikando A, Lederer WJ
    Ca(2+) signaling is of vital importance to cardiac cell function and plays an important role in heart failure. It is based on sarcolemmal, sarcoplasmic reticulum and mitochondrial Ca(2+) cycling. While the first two are well characterized, the latter remains unclear, controversial and technically challenging. In mammalian cardiac myocytes, Ca(2+) influx through L-type calcium channels in the sarcolemmal membrane triggers Ca(2+) release from the nearby junctional sarcoplasmic reticulum to produce Ca(2+) sparks. When this triggering is synchronized by the cardiac action potential, a global [Ca(2+)](i) transient arises from coordinated Ca(2+) release events. The ends of intermyofibrillar mitochondria are located within 20 nm of the junctional ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734954</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:19 +0100</pubDate>
            <guid isPermaLink="false">2734954</guid>        </item>
        <item>
            <title>Use of NADH fluorescence to determine mitochondrial function in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=2734953&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703658%26dopt%3DAbstract</link>
            <description>Authors: Mayevsky A, Barbiro-Michaely E
    Normal mitochondrial function is a critical factor in maintaining cellular homeostasis in various organs of the body. Due to the involvement of mitochondrial dysfunction in many pathological states, the real-time in vivo monitoring of the mitochondrial metabolic state is crucially important. This type of monitoring in animal models as well as in patients provides real-time data that can help interpret experimental results or optimize patient treatment. In this paper we are summarizing the following items: (1) presenting the solid scientific ground underlying nicotine amide adenine dinucleotide (NADH) NADH fluorescence measurements based on published materials. (2) Presenting NADH fluorescence monitoring and its physiological significance. (3) Pro...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734953</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:17 +0100</pubDate>
            <guid isPermaLink="false">2734953</guid>        </item>
        <item>
            <title>Brain mitochondria as a primary target in the development of treatment strategies for Alzheimer disease.</title>
            <link>http://www.medworm.com/index.php?rid=2734952&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703659%26dopt%3DAbstract</link>
            <description>Authors: Aliev G, Palacios HH, Walrafen B, Lipsitt AE, Obrenovich ME, Morales L
    Alzheimer's disease (AD) and cerebrovascular accidents are two leading causes of age-related dementia. Increasing evidence supports the idea that chronic hypoperfusion is primarily responsible for the pathogenesis that underlies both disease processes. In this regard, hypoperfusion appears to induce oxidative stress (OS), which is largely due to reactive oxygen species (ROS), and over time initiates mitochondrial failure which is known as an initiating factor of AD. Recent evidence indicates that chronic injury stimulus induces hypoperfusion seen in vulnerable brain regions. This reduced regional cerebral blood flow (CBF) then leads to energy failure within the vascular endothelium and associated brain pare...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734952</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:14 +0100</pubDate>
            <guid isPermaLink="false">2734952</guid>        </item>
        <item>
            <title>The role of PTEN-induced kinase 1 in mitochondrial dysfunction and dynamics.</title>
            <link>http://www.medworm.com/index.php?rid=2734951&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703660%26dopt%3DAbstract</link>
            <description>Authors: Thomas KJ, Cookson MR
    Mutations in parkin, PTEN-induced kinase 1 (PINK1) and DJ-1 can all cause autosomal recessive forms of Parkinson's disease. Recent data suggest that these recessive parkinsonism-associated genes converge within a single pathogenic pathway whose dysfunction leads to the loss of substantia nigra pars compacta neurons. The major common functional effects of all three genes relate to mitochondrial and oxidative damage, with a possible additional involvement of the ubiquitin proteasome system. This review highlights the role of the mitochondrial kinase, PINK1, in protection against mitochondrial dysfunction and how this might relate to loss of substantia nigra neurons in recessive parkinsonism.
    PMID: 19703660 [PubMed - in process] (Source: The Internationa...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734951</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:11 +0100</pubDate>
            <guid isPermaLink="false">2734951</guid>        </item>
        <item>
            <title>Glutamine homeostasis and mitochondrial dynamics.</title>
            <link>http://www.medworm.com/index.php?rid=2734950&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703661%26dopt%3DAbstract</link>
            <description>Authors: Mat&amp;#xE9;s JM, Segura JA, Campos-Sandoval JA, Lobo C, Alonso L, Alonso FJ, M&amp;#xE1;rquez J
    Glutamine is a multifaceted amino acid that plays key roles in many metabolic pathways and also fulfils essential signaling functions. Although classified as non-essential, recent evidence suggests that glutamine is a conditionally essential amino acid in several physiological situations. Glutamine homeostasis must therefore be exquisitely regulated and mitochondria represent a major site of glutamine metabolism in numerous cell types. Glutaminolysis is mostly a mitochondrial process with repercussions in organelle structure and dynamics suggesting a tight and mutual control between mitochondrial form and cell bioenergetics. In this review we describe an updated account focused on the cri...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734950</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:08 +0100</pubDate>
            <guid isPermaLink="false">2734950</guid>        </item>
        <item>
            <title>Electron microscopy morphology of the mitochondrial network in human cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2734949&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19703662%26dopt%3DAbstract</link>
            <description>Authors: Arismendi-Morillo G
    Mitochondria have been implicated in the process of carcinogenesis, which includes alterations of cellular metabolism and cell death pathways. The aim of this review is to describe and analyze the electron microscopy morphology of the mitochondrial network in human cancer. The structural mitochondrial alterations in human tumors are heterogeneous and not specific for any neoplasm. These findings could be representing an altered structural and functional mitochondrial network. The mitochondria in cancer cells, independently of histogenesis, predominantly are seen with lucent-swelling matrix associated with disarrangement and distortion of cristae and partial or total cristolysis and with condensed configuration in minor scale. Mitochondrial changes are assoc...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734949</comments>
            <pubDate>Thu, 27 Aug 2009 02:30:06 +0100</pubDate>
            <guid isPermaLink="false">2734949</guid>        </item>
        <item>
            <title>Granulocyte colony-stimulating factor receptor: stimulating granulopoiesis and much more.</title>
            <link>http://www.medworm.com/index.php?rid=2734964&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19699815%26dopt%3DAbstract</link>
            <description>Authors: Liongue C, Wright C, Russell AP, Ward AC
    The granulocyte colony-stimulating factor receptor (G-CSFR) plays an important role in the production, survival and activation of neutrophilic granulocytes during both normal and emergency hematopoiesis. The G-CSFR also participates in the production development of other myeloid lineages, the mobilization of hematopoietic stem cells and myeloid cell migration. This has lead to several important clinical applications for its ligand, G-CSF. More recently, additional important roles for G-CSFR have emerged outside the hematopoietic system, such as in the protection and repair of a diverse range of tissues, including muscle, liver and neural tissue, providing further scope for developing G-CSF as a therapeutic agent. The G-CSFR has also bee...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2734964</comments>
            <pubDate>Wed, 19 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2734964</guid>        </item>
        <item>
            <title>Patt1, a novel protein acetyltransferase that is highly expressed in liver and downregulated in hepatocellular carcinoma, enhances apoptosis of hepatoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=2723564&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19695338%26dopt%3DAbstract</link>
            <description>In this study, we identified a novel protein acetyltransferase, Patt1, which belongs to GNAT family. Patt1 exhibited histone acetyltransferase activity and auto-acetylation activity. Deletion and mutation analysis of the predicted acetyltransferase domain in Patt1 showed that the conserved Glu139 was an important residue for its protein acetyltransferase activity. Furthermore, we found that Patt1 was highly expressed in liver and significantly downregulated in hepatocellular carcinoma tissues. In addition, we showed that overexpression of Patt1 enhanced the apoptosis of hepatoma cells dependent on its acetyltransferase activity, whereas knockdown of Patt1 significantly protected Chang liver cells from apoptosis. These data suggest that Patt1 might be involved in the development of hepatoce...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723564</comments>
            <pubDate>Sun, 16 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723564</guid>        </item>
        <item>
            <title>Endoplasmic Reticulum stress reduces the export from the ER and alters the architecture of post-ER compartments.</title>
            <link>http://www.medworm.com/index.php?rid=2723563&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19695339%26dopt%3DAbstract</link>
            <description>Authors: Amodio G, Renna M, Paladino S, Venturi C, Tacchetti C, Moltedo O, Franceschelli S, Mallardo M, Bonatti S, Remondelli P
    In eukaryotic cells several physiologic and pathologic conditions generate the accumulation of unfolded proteins in the endoplasmic reticulum (ER), leading to ER stress. To restore normal function, some ER transmembrane proteins sense the ER stress and activate coordinated signalling pathways collectively called the Unfolded Protein Response (UPR). Little is known on how the UPR relates to post-ER compartments and to the export from the ER of newly synthesized proteins. Here, we report that the ER stress response induced by either thapsigargin or nitric oxide modifies the dynamics of the intracellular distribution of ERGIC-53 and GM130, two markers of the ER-G...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723563</comments>
            <pubDate>Sun, 16 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723563</guid>        </item>
        <item>
            <title>Effect of Peroxynitrite on Endothelial L-Arginine Transport and Metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=2723562&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19695340%26dopt%3DAbstract</link>
            <description>Conclusion: Peroxynitrite negatively influences NO production by combined effects on arginine uptake and efflux, most likely due to a nitrosative action of ONOO(-) on CAT-1.
    PMID: 19695340 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723562</comments>
            <pubDate>Sun, 16 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723562</guid>        </item>
        <item>
            <title>Polyamine modulon in yeast - Stimulation of COX4 synthesis by spermidine at the level of translation.</title>
            <link>http://www.medworm.com/index.php?rid=2723561&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19695341%26dopt%3DAbstract</link>
            <description>Authors: Uemura T, Higashi K, Takigawa M, Toida T, Kashiwagi K, Igarashi K
    We proposed that a group of genes whose expression is enhanced by polyamines at the level of translation in Escherichia coli and mammalian cells be referred to as a &quot;polyamine modulon&quot;. In Saccharomyces cerevisiae, proteins whose synthesis is enhanced by polyamines at the level of translation were searched for using a polyamine-requiring mutant of S. cerevisiae deficient in ornithine decarboxylase (YPH499 Deltaspe1). Addition of spermidine to the medium recovered the spermidine content and enhanced cell growth of the YPH499 Deltaspe1 mutant by 3- to 5-fold. Under these conditions, synthesis of COX4, one of the subunits of cytochrome C oxidase (complex IV), was enhanced by polyamines about 2.5-fold at the level o...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723561</comments>
            <pubDate>Sun, 16 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723561</guid>        </item>
        <item>
            <title>Ricin A-chain requires c-Jun N-terminal kinase to induce apoptosis in nontransformed epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=2723560&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19695342%26dopt%3DAbstract</link>
            <description>Authors: Jetzt AE, Cheng JS, Tumer NE, Cohick WS
    Ricin is a toxin isolated from castor beans that has potential as a weapon of bioterrorism. This glycoprotein consists of an A-chain (RTA) that damages the ribosome and inhibits protein synthesis and a B-chain that plays a role in cellular uptake. Ricin activates the c-Jun N-terminal kinase (JNK) and p38 signaling pathways; however, a role for these pathways in ricin-induced cell death has not been investigated. Our goals were to determine if RTA alone could activate apoptosis and if the JNK and p38 pathways were required for this response. Comparable caspase activation was observed with both ricin and RTA treatment in the immortalized, nontransformed epithelial cell line, MAC-T. Ribosome depurination and inhibition of protein synthesis ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2723560</comments>
            <pubDate>Sun, 16 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2723560</guid>        </item>
        <item>
            <title>The resveratrol analogue 4,4'-dihydroxy-trans-stilbene inhibits cell proliferation with higher efficiency but different mechanism from resveratrol.</title>
            <link>http://www.medworm.com/index.php?rid=2702986&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19679195%26dopt%3DAbstract</link>
            <description>In conclusion, 4,4'-di-hydroxy-trans-stilbene has potent antiproliferative activities that differ from the effect of resveratrol shown in this system, suggesting that it warrants further development as a potential chemopreventive or therapeutic agent.
    PMID: 19679195 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2702986</comments>
            <pubDate>Sun, 09 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2702986</guid>        </item>
        <item>
            <title>ATP STIMULATES Ca(2+)-WAVES AND GENE EXPRESSION IN CULTURED HUMAN PULMONARY FIBROBLASTS.</title>
            <link>http://www.medworm.com/index.php?rid=2696652&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19666134%26dopt%3DAbstract</link>
            <description>Authors: Janssen LJ, Farkas L, Rahman T, Kolb MR
    Given that extracellular ATP is markedly elevated in inflammation and is known to modulate fibroblast function, we examined the effects of exogenously-added ATP on Ca(2+)-handling and gene expression in human pulmonary fibroblasts. Cells were loaded with the Ca(2+)-indicator dye fluo-4 and studied using confocal fluorimetry. Standard RT-PCR was used to probe gene expression. ATP (10(-5) M) evoked recurring Ca(2+)-waves which were completely occluded by cyclopiazonic acid (depletes the internal Ca(2+)-store) or the phospholipase inhibitor U73122. Pretreatment with ryanodine (10(-5) M), however, had no effect on the ATP-evoked responses. Regarding the receptor through which ATP acted, we found the ATP-response to be mimicked by UTP or ADP ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2696652</comments>
            <pubDate>Thu, 06 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2696652</guid>        </item>
        <item>
            <title>Proteomic and biochemical analyses unveil tight interaction of ataxin-3 with tubulin.</title>
            <link>http://www.medworm.com/index.php?rid=2696651&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19666135%26dopt%3DAbstract</link>
            <description>Authors: Mazzucchelli S, De Palma A, Riva M, D'Urzo A, Pozzi C, Pastori V, Comelli F, Fusi P, Vanoni M, Tortora P, Mauri P, Regonesi ME
    Ataxin-3 consists of an N-terminal globular Josephin domain and an unstructured C-terminal region containing a stretch of consecutive glutamines that triggers an inherited neurodegenerative disorder, spinocerebellar ataxia type 3, when its length exceeds a critical threshold. The pathology results from protein misfolding and intracellular accumulation of fibrillar amyloid-like aggregates. Plenty of work has been carried out to elucidate the protein's physiological role(s), which has shown that ataxin-3 is multifunctional; it acts as a transcriptional repressor, and also has polyubiquitin-binding/ubiquitin hydrolase activity. In addition, a recent repor...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2696651</comments>
            <pubDate>Thu, 06 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2696651</guid>        </item>
        <item>
            <title>Colon cancer metastasis: MACC1 and Met as metastatic pacemakers.</title>
            <link>http://www.medworm.com/index.php?rid=2696650&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19666136%26dopt%3DAbstract</link>
            <description>Authors: Arlt F, Stein U
    Colon cancer is still the second most frequent malignancy in the Western world. Despite major efforts in diagnosis and treatment it is one of the leading causes of cancer related deaths. The metastatic dissemination of primary tumors is directly linked to patient's survival and accounts for about 90% of all colon cancer deaths. Current clinical predictions on whether colon cancer will metastasize are mainly defined by histopathological staging, describing the tumor spread within a surgical specimen. This review focuses on the need for molecular-based staging as essential prerequisite for individualized diagnosis, prognosis and therapy. Molecular determinants for progression and metastasis of colon cancer are discussed. Moreover, a newly identified molecule play...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2696650</comments>
            <pubDate>Thu, 06 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2696650</guid>        </item>
        <item>
            <title>Cardiac Hypertrophy: Targeting Raf/MEK/ERK1/2-Signaling.</title>
            <link>http://www.medworm.com/index.php?rid=2696649&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19666137%26dopt%3DAbstract</link>
            <description>Authors: Lorenz K, Schmitt JP, Vidal M, Lohse MJ
    Over the past two decades, basic research has revealed a complex network of regulatory mechanisms that control the ERK1/2 signaling cascade. ERK1/2 mediate cardiac hypertrophy, a major risk factor for the development of arrhythmias, heart failure and sudden death, but also beneficial effects, e.g. protection of the heart from cell death and ischemic injury. Selective targeting of these ambiguous ERK functions could provide a powerful tool in the treatment of cardiac disease. This short review will discuss new mechanistic insights into ERK1/2-dependent development of cardiac hypertrophy and the prospect to translate this knowledge into future therapeutic strategies.
    PMID: 19666137 [PubMed - as supplied by publisher] (Source: The Inter...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2696649</comments>
            <pubDate>Thu, 06 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2696649</guid>        </item>
        <item>
            <title>miR-584 mediates post-transcriptional expression of lactoferrin receptor in Caco-2 cells and in mouse small intestine during the perinatal period.</title>
            <link>http://www.medworm.com/index.php?rid=2696653&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19665576%26dopt%3DAbstract</link>
            <description>The objective of this study was to identify mechanisms of microRNA mediated post-transcriptional regulation of the lactoferrin receptor. Sequence analyses revealed that the miR-584 sequence is identical in human, mouse and rat, and there is a conserved region complementary to the seed region (5' nucleotides 2-8) of miR-584 within the lactoferrin receptor mRNA-3' untranslated region. miR-584 was further found to co-localize with lactoferrin receptor mRNA in mouse small intestine. The 3' untranslated region of human lactoferrin receptor mRNA was cloned into pGL3-control luciferase reporter vector. By luciferase reporter assays in HEK293 cells, miR-584 mimic specifically repressed the reporter activity in a dose-dependent manner. miR-584 mimic reduced endogenous lactoferrin receptor protein e...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2696653</comments>
            <pubDate>Wed, 05 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2696653</guid>        </item>
        <item>
            <title>Role of non-neuronal nicotinic acetylcholine receptors in angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2547039&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401144%26dopt%3DAbstract</link>
            <description>Authors: Arias HR, Richards VE, Ng D, Ghafoori ME, Le V, Mousa SA
    Angiogenesis is a critical physiological process for cell survival and development. Endothelial cells, necessary for the course of angiogenesis, express several non-neuronal nicotinic acetylcholine receptors (AChRs). The most important functional non-neuronal AChRs are homomeric alpha7 AChRs and several heteromeric AChRs formed by a combination of alpha3, alpha5, beta2, and beta4 subunits, including alpha3beta4-containing AChRs. In endothelial cells, alpha7 AChR stimulation indirectly triggers the activation of the integrin alphavbeta3 receptor and an intracellular MAP kinase (ERK) pathway that mediates angiogenesis. Non-selective cholinergic agonists such as nicotine have been shown to induce angiogenesis, enhancing tum...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547039</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:54 +0100</pubDate>
            <guid isPermaLink="false">2547039</guid>        </item>
        <item>
            <title>Revisiting the seed and soil in cancer metastasis.</title>
            <link>http://www.medworm.com/index.php?rid=2547037&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401145%26dopt%3DAbstract</link>
            <description>Authors: Mendoza M, Khanna C
    Metastasis remains the overwhelming cause of death for cancer patients. During metastasis, cancer cells will leave the primary tumor, intravasate into the bloodstream, arrest at a distant organ, and eventually develop into gross lesions at the secondary sites. This intricate process is influenced by innumerable factors and complex cellular interactions described in 1889 by Stephen Paget as the seed and soil hypothesis. In this review, we revisit this seed and soil hypothesis with an emerging understanding of the cancer cell (i.e. seed) and its microenvironment (i.e. soil). We will provide background to suggest that a critical outcome of the seed-soil interaction is resistance of the stresses that would otherwise impede metastasis.
    PMID: 19401145 [PubMed...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547037</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:52 +0100</pubDate>
            <guid isPermaLink="false">2547037</guid>        </item>
        <item>
            <title>Citicoline (CDP-choline): What role in the treatment of complications of infectious diseases.</title>
            <link>http://www.medworm.com/index.php?rid=2547035&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401146%26dopt%3DAbstract</link>
            <description>Authors: Jambou R, El-Assaad F, Combes V, Grau GE
    A dysregulated host immune response, as opposed to the intrinsic virulence of a microbial pathogen induces a large part of the pathology seen in infectious diseases. However, current therapies are designed to target the pathogen rather than the underlying pathogenic mechanisms responsible for the manifestation of the pathology. Recent studies have highlighted the role of endothelial cell alteration in the pathology induced in sepsis and cerebral malaria. The endothelial onslaught described, is similar to that seen during ischemia reperfusion in stroke. Protecting endothelial cell membranes during sepsis and cerebral malaria, using citicoline in the same way as in stroke, has thus emerged as a new strategy that needs to be evaluated urge...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547035</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:49 +0100</pubDate>
            <guid isPermaLink="false">2547035</guid>        </item>
        <item>
            <title>Protein-protein interactions involving voltage-gated sodium channels: Post-translational regulation, intracellular trafficking and functional expression.</title>
            <link>http://www.medworm.com/index.php?rid=2547033&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401147%26dopt%3DAbstract</link>
            <description>Authors: Shao D, Okuse K, Djamgoz MB
    Voltage-gated sodium channels (VGSCs), classically known to play a central role in excitability and signalling in nerves and muscles, have also been found to be expressed in a range of 'non-excitable' cells, including lymphocytes, fibroblasts and endothelia. VGSC abnormalities are associated with various diseases including epilepsy, long-QT syndrome 3, Brugada syndrome, sudden infant death syndrome and, more recently, various human cancers. Given their pivotal role in a wide range of physiological and pathophysiological processes, regulation of functional VGSC expression has been the subject of intense study. An emerging theme is post-translational regulation and macro-molecular complexing by protein-protein interactions and intracellular traffickin...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547033</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:47 +0100</pubDate>
            <guid isPermaLink="false">2547033</guid>        </item>
        <item>
            <title>Transaldolase: from biochemistry to human disease.</title>
            <link>http://www.medworm.com/index.php?rid=2547031&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401148%26dopt%3DAbstract</link>
            <description>Authors: Samland AK, Sprenger GA
    The role of the enzyme transaldolase (TAL) in central metabolism, its biochemical properties, structure, and role in human disease is reviewed. The nearly ubiquitous enzyme transaldolase is a part of the pentose phosphate pathway and transfers a dihydroxyacetone group from donor compounds (fructose 6-phosphate or sedoheptulose 7-phosphate) to aldehyde acceptor compounds. The phylogeny of transaldolases shows that five subfamilies can be distinguished, three of them with proven TAL enzyme activity, one with unclear function, and the fifth subfamily comprises transaldolase-related enzymes, the recently discovered fructose 6-phosphate aldolases. The three-dimensional structure of a bacterial (Escherichia coli TAL B) and the human enzyme (TALDO1) has been s...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547031</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:44 +0100</pubDate>
            <guid isPermaLink="false">2547031</guid>        </item>
        <item>
            <title>Native HMGB1 protein inhibits repair of cisplatin-damaged nucleosomes in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=2547029&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401149%26dopt%3DAbstract</link>
            <description>Authors: Ugrinova I, Zlateva S, Pashev IG, Pasheva EA
    The high mobility group box (HMGB) 1 protein, one of the most abundant nuclear non-histone proteins has been known for its inhibitory effect on repair of DNA damaged by the antitumor drug cisplatin. Here, we report the first results that link HMGB1 to repair of cisplatin-treated DNA at nucleosome level. Experiments were carried out with three types of reconstituted nucleosomes strongly positioned on the damaged DNA: linker DNA containing nucleosomes (centrally and end-positioned) and core particles. The highest repair synthesis was registered with end-positioned nucleosomes, two and three times more efficient than that with centrally positioned nucleosomes and core particles, respectively. HMGB1 inhibited repair of linker DNA contai...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547029</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:42 +0100</pubDate>
            <guid isPermaLink="false">2547029</guid>        </item>
        <item>
            <title>Differences in hydroxylation and binding of Notch and HIF-1alpha demonstrate substrate selectivity for factor inhibiting HIF-1 (FIH-1).</title>
            <link>http://www.medworm.com/index.php?rid=2547027&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401150%26dopt%3DAbstract</link>
            <description>Authors: Wilkins SE, Hyv&amp;#xE4;rinen J, Chicher J, Gorman JJ, Peet DJ, Bilton RL, Koivunen P
    FIH-1, factor inhibiting hypoxia-inducible factor-1 (HIF-1), regulates oxygen sensing by hydroxylating an asparagine within HIF-alpha. It also hydroxylates asparagines in many proteins containing ankyrin repeats, including Notch1-3, p105 and I?B?. Relative binding affinity and hydroxylation rate are crucial determinants of substrate selection and modification. We determined the contributions of substrate sequence composition and length and of oxygen concentration to the FIH-1-binding and/or hydroxylation of Notch1-4 and compared them with those for HIF-1alpha. We also demonstrated hydroxylation of two asparagines in Notch2 and 3, corresponding to Sites 1 and 2 of Notch1, by mass spectrometry for...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547027</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:39 +0100</pubDate>
            <guid isPermaLink="false">2547027</guid>        </item>
        <item>
            <title>The soluble form of the cancer-associated L1 cell adhesion molecule is a pro-angiogenic factor.</title>
            <link>http://www.medworm.com/index.php?rid=2547025&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401151%26dopt%3DAbstract</link>
            <description>In this study we describe a novel function of this physiologically relevant form of L1 as a pro-angiogenic factor. We demonstrated that the anti-L1 monoclonal antibody (mAb) chCE7 binds near or to the sixth Ig-like domain of human L1 which contains a single RGD sequence. mAb chCE7 inhibited the RGD-dependent adhesion of ovarian carcinoma cells to sL1 and reversed the sL1-induced proliferation, matrigel invasion and tube formation of bovine aortic endothelial (BAE) cells. A combination of sL1 with vascular endothelial growth factor-A (VEGF-A(165)), which is an important angiogenic inducer in tumors, strongly potentiated VEGF receptor-2 tyrosine phosphorylation in BAE cells. Chick chorioallantoic membrane (CAM) assays revealed the pro-angiogenic potency of sL1 in vivo which could be abolishe...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547025</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:37 +0100</pubDate>
            <guid isPermaLink="false">2547025</guid>        </item>
        <item>
            <title>Evidence for aerobic ATP synthesis in isolated myelin vesicles.</title>
            <link>http://www.medworm.com/index.php?rid=2547023&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401152%26dopt%3DAbstract</link>
            <description>Authors: Ravera S, Panfoli I, Calzia D, Aluigi MG, Bianchini P, Diaspro A, Mancardi G, Morelli A
    Even though brain represents only 2-3% of the body weight, it consumes 20% of total body oxygen, and 25% of total body glucose. This sounds surprising, in that mitochondrial density in brain is low, while mitochondria are thought to be the sole site of aerobic energy supply. These data would suggest that structures other than mitochondria are involved in aerobic ATP production. Considering that a sustained aerobic metabolism needs a great surface extension and that the oxygen solubility is higher in neutral lipids, we have focused our attention on myelin sheath, the multilayered membrane produced by oligodendrocytes, hypothesizing it to be an ATP production site. Myelin has long been suppos...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547023</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:34 +0100</pubDate>
            <guid isPermaLink="false">2547023</guid>        </item>
        <item>
            <title>Activation of phosphatidylinositol 3-kinase is required for tumor necrosis factor-alpha-induced upregulation of matrix metalloproteinase-9: its direct inhibition by quercetin.</title>
            <link>http://www.medworm.com/index.php?rid=2547021&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401153%26dopt%3DAbstract</link>
            <description>Authors: Hwang MK, Song NR, Kang NJ, Lee KW, Lee HJ
    Matrix metalloproteinases (MMPs) are involved in various skin disorders, including photoaging, dermatitis, and tumorigenesis. Tumor necrosis factor (TNF)-alpha is a key proinflammatory cytokine that acts to provoke inflammation, proliferation, and tumorigenesis. The present study investigated the possible inhibitory effects of red wine polyphenols on TNF-alpha-induced upregulation of MMP-9 and on the migratory phenotype of JB6 P+ mouse epidermal (JB6 P+) cells. Red wine extract (RWE) and quercetin, which is a major flavonoid present in red wine, inhibited significantly the TNF-alpha-induced upregulation of MMP-9 and cell migration, whereas resveratrol did not have significant inhibitory effects. The inhibitory effects of RWE and querc...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547021</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:32 +0100</pubDate>
            <guid isPermaLink="false">2547021</guid>        </item>
        <item>
            <title>A major cathepsin B protease from the liver fluke Fasciola hepatica has atypical active site features and a potential role in the digestive tract of newly excysted juvenile parasites.</title>
            <link>http://www.medworm.com/index.php?rid=2547019&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401154%26dopt%3DAbstract</link>
            <description>Authors: Beckham SA, Piedrafita D, Phillips CI, Samarawickrema N, Law RH, Smooker PM, Quinsey NS, Irving JA, Greenwood D, Verhelst SH, Bogyo M, Turk B, Coetzer TH, Wijeyewickrema LC, Spithill TW, Pike RN
    The newly excysted juvenile (NEJ) stage of the Fasciola hepatica lifecycle occurs just prior to invasion into the wall of the gut of the host, rendering it an important target for drug development. The cathepsin B enzymes from NEJ flukes have recently been demonstrated to be crucial to invasion and migration by the parasite. Here we characterize one of the cathepsin B enzymes (recombinant FhcatB1) from NEJ flukes. FhcatB1 has biochemical properties distinct from mammalian cathepsin B enzymes, with an atypical preference for Ile over Leu or Arg residues at the P(2) substrate position an...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547019</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:30 +0100</pubDate>
            <guid isPermaLink="false">2547019</guid>        </item>
        <item>
            <title>Four and a half LIM domains 1 (FHL1) and receptor interacting protein of 140kDa (RIP140) interact and cooperate in estrogen signaling.</title>
            <link>http://www.medworm.com/index.php?rid=2547017&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401155%26dopt%3DAbstract</link>
            <description>Authors: Lin J, Ding L, Jin R, Zhang H, Cheng L, Qin X, Chai J, Ye Q
    Four and a half LIM domains 1 (FHL1) belongs to a family of LIM-only proteins that regulate gene transcription, cell proliferation, differentiation and apoptosis. However, the biological function of FHL1 remains largely unknown. We used a yeast two-hybrid system and identified receptor interacting protein of 140kDa (RIP140) as a novel FHL1-binding protein. RIP140 interacted with FHL1 both in vitro and in mammalian cells and estrogen enhanced this interaction. All domains of FHL1 are required to interact with RIP140. Overexpression of FHL1 enhanced RIP140 repression of estrogen signaling in breast cancer cells in a reporter assay, whereas reduction of endogenous FHL1 with FHL1 small interfering RNA abolished this effec...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547017</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:27 +0100</pubDate>
            <guid isPermaLink="false">2547017</guid>        </item>
        <item>
            <title>COP-binding sites in p24delta2 are necessary for proper secretory cargo biosynthesis.</title>
            <link>http://www.medworm.com/index.php?rid=2547015&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401156%26dopt%3DAbstract</link>
            <description>Authors: Strating JR, Hafmans TG, Martens GJ
    The p24 family is thought to be somehow involved in endoplasmic reticulum-to-Golgi protein transport, and its members are major constituents of transport vesicles and bind to the vesicle coat protein complexes COPI and COPII. A subset of the p24 proteins (p24alpha(3), -beta(1), -gamma(3) and -delta(2)) is upregulated when Xenopus laevis intermediate pituitary melanotrope cells are physiologically activated to produce vast amounts of their major secretory cargo, the prohormone proopiomelanocortin (POMC). To investigate the role of the COP-binding motifs of p24 proteins in POMC biosynthesis, we here generated and analysed Xenopus with stable, melanotrope cell-specific transgene expression of p24delta(2)-GFP mutated in its COPI- or COPII-bindin...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547015</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:25 +0100</pubDate>
            <guid isPermaLink="false">2547015</guid>        </item>
        <item>
            <title>Comparative expression analysis reveals differences in the regulation of intestinal paraoxonase family members.</title>
            <link>http://www.medworm.com/index.php?rid=2547013&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19401157%26dopt%3DAbstract</link>
            <description>This study was designed to determine the regulation of PONs by oxidative stress and inflammatory factors. Differentiated Caco-2/15 cells, cultured on polycarbonate Transwell filter inserts, exhibited transcripts of the 3 PONs whereas Western blot revealed the protein expression of PON2 and PON3 only. Iron-ascorbate-mediated lipid peroxidation, lipopolysaccharides (LPS), tumor necrosis factor-alpha and interferon-gamma induced differential effects on the gene expression and protein mass of PONs. In particular, LPS down-regulated PON2 protein expression, which was accompanied with decreased levels of IkappaBalpha, the inhibitor of the proinflammatory transcription factor nuclear factor-kappa B (NF-kappaB). Selective inactivation of NF-kappaB by the action of caffeic acid phenethyl ester (CAP...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547013</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:22 +0100</pubDate>
            <guid isPermaLink="false">2547013</guid>        </item>
        <item>
            <title>Hepatic stellate cell: a star cell in the liver.</title>
            <link>http://www.medworm.com/index.php?rid=2547000&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433304%26dopt%3DAbstract</link>
            <description>Authors: Atzori L, Poli G, Perra A
    Hepatic stellate cells represent a highly versatile cytotype that plays a significant role in liver development and differentiation, regeneration, xenobiotic response, immunoregulation, control of hepatic blood flow and inflammatory reactions. Because of the wide panel of molecular intermediates they may produce and secrete, particularly after their sustained activation in a disease state, hepatic stellate cells are definitely involved in the pathogenesis of various liver pathologies, besides the well know key role in fibrosis and extracellular matrix remodelling. In particular, they can actively contribute to the progression of hepatitis and steatohepatitis of different aetiology, and of liver carcinogenesis.
    PMID: 19433304 [PubMed - indexed for ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2547000</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:06 +0100</pubDate>
            <guid isPermaLink="false">2547000</guid>        </item>
        <item>
            <title>Lung alveolar epithelium and interstitial lung disease.</title>
            <link>http://www.medworm.com/index.php?rid=2546998&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433305%26dopt%3DAbstract</link>
            <description>Authors: Corvol H, Flamein F, Epaud R, Clement A, Guillot L
    Interstitial lung diseases (ILDs) comprise a group of lung disorders characterized by various levels of inflammation and fibrosis. The current understanding of the mechanisms underlying the development and progression of ILD strongly suggests a central role of the alveolar epithelium. Following injury, alveolar epithelial cells (AECs) may actively participate in the restoration of a normal alveolar architecture through a coordinated process of re-epithelialization, or in the development of fibrosis through a process known as epithelial-mesenchymal transition (EMT). Complex networks orchestrate EMT leading to changes in cell architecture and behaviour, loss of epithelial characteristics and gain of mesenchymal properties. In th...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546998</comments>
            <pubDate>Sun, 28 Jun 2009 04:03:01 +0100</pubDate>
            <guid isPermaLink="false">2546998</guid>        </item>
        <item>
            <title>Cyclophilin 40: an Hsp90-cochaperone associated with apo-steroid receptors.</title>
            <link>http://www.medworm.com/index.php?rid=2546996&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433306%26dopt%3DAbstract</link>
            <description>Authors: Ratajczak T, Ward BK, Cluning C, Allan RK
    Cyclophilin 40, a divergent loop cyclophilin first identified in association with the estrogen receptor alpha, contains a C-terminal tetratricopeptide repeat domain through which it shares structural identity with FK506-binding protein 52 (FKBP52) and other partner cochaperones in steroid receptor-heat shock protein 90 (Hsp90) complexes. By dynamically competing for Hsp90 interaction, the cochaperones allow the receptors to establish distinct Hsp90-chaperone complexes, with the potential to exert tissue-specific control over receptor activity. Cyclophilin 40 regulates Hsp90 ATPase activity during receptor-Hsp90 assembly. Functional deletion of the cyclophilin 40 yeast homologue, Cpr7, adversely affected estrogen receptor alpha and gluc...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546996</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:56 +0100</pubDate>
            <guid isPermaLink="false">2546996</guid>        </item>
        <item>
            <title>Filopodia: Complex models for simple rods.</title>
            <link>http://www.medworm.com/index.php?rid=2546994&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433307%26dopt%3DAbstract</link>
            <description>Authors: Faix J, Breitsprecher D, Stradal TE, Rottner K
    Filopodia are prominent cell surface projections filled with bundles of linear actin filaments that drive their protrusion. These structures are considered important sensory organelles, for instance in neuronal growth cones or during the fusion of sheets of epithelial tissues. In addition, they can serve a precursor function in adhesion site or stress fibre formation. Actin filament assembly is essential for filopodia formation and turnover, yet the precise molecular mechanisms of filament nucleation and/or elongation are controversial. Indeed, conflicting reports on the molecular requirements of filopodia initiation have prompted researchers to propose different types and/or alternative or redundant mechanisms mediating this proc...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546994</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:52 +0100</pubDate>
            <guid isPermaLink="false">2546994</guid>        </item>
        <item>
            <title>The biochemistry of environmental heavy metal uptake by plants: implications for the food chain.</title>
            <link>http://www.medworm.com/index.php?rid=2546992&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433308%26dopt%3DAbstract</link>
            <description>Authors: Peralta-Videa JR, Lopez ML, Narayan M, Saupe G, Gardea-Torresdey J
    Plants absorb a number of elements from soil, some of which have no known biological function and some are known to be toxic at low concentrations. As plants constitute the foundation of the food chain, some concerns have been raised about the possibility of toxic concentrations of certain elements being transported from plants to higher strata of the food chain. Special attention has been given to the uptake and biotransformation mechanisms occurring in plants and its role in bioaccumulation and impact on consumers, especially human beings. While this review draws particular attention to metal accumulation in edible plants, researched studies of certain wild plants and their consumers are included. Furthermore...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546992</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:46 +0100</pubDate>
            <guid isPermaLink="false">2546992</guid>        </item>
        <item>
            <title>Nuclear localization of c-FLIP-L and its regulation of AP-1 activity.</title>
            <link>http://www.medworm.com/index.php?rid=2546990&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433309%26dopt%3DAbstract</link>
            <description>In this report, we showed for the first time that c-FLIP-L was present in both the cytoplasm and nucleus of cells, but was more abundantly distributed in the nucleus. The putative NLS signal locates within the p12 region of caspase-like domain. Furthermore, c-FLIP's export to cytoplasm membrane was dependent on apoptotic stimulation, while it rapidly translocated to the nucleus in response to proliferative stimuli. To gain insights into the possible function of c-FLIP-L in the nucleus, we found c-FLIP-L could activate the AP-1 transcriptional activity independent of MAPK activation. In sum, our findings describe a novel function of c-FLIP-L involved in AP-1 activation and cell proliferation.
    PMID: 19433309 [PubMed - indexed for MEDLINE] (Source: The International Journal of Biochemistr...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546990</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:44 +0100</pubDate>
            <guid isPermaLink="false">2546990</guid>        </item>
        <item>
            <title>Cathepsin X cleaves the C-terminal dipeptide of alpha- and gamma-enolase and impairs survival and neuritogenesis of neuronal cells.</title>
            <link>http://www.medworm.com/index.php?rid=2546988&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433310%26dopt%3DAbstract</link>
            <description>In this study we identify isozymes alpha- and gamma-enolases as targets for cathepsin X. Cathepsin X sequentially cleaves C-terminal amino acids of both isozymes, abolishing their neurotrophic activity. Neuronal cell survival and neuritogenesis are, in this way, regulated, as shown on pheochromocytoma cell line PC12. Inhibition of cathepsin X activity increases generation of plasmin, essential for neuronal differentiation and changes the length distribution of neurites, especially in the early phase of neurite outgrowth. Moreover, cathepsin X inhibition increases neuronal survival and reduces serum deprivation induced apoptosis, particularly in the absence of nerve growth factor. On the other hand, the proliferation of cells is decreased, indicating induction of differentiation. Our study ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546988</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:41 +0100</pubDate>
            <guid isPermaLink="false">2546988</guid>        </item>
        <item>
            <title>Pro-oxidant mitochondrial matrix-targeted ubiquinone MitoQ10 acts as anti-oxidant at retarded electron transport or proton pumping within Complex I.</title>
            <link>http://www.medworm.com/index.php?rid=2546986&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433311%26dopt%3DAbstract</link>
            <description>Authors: Plecit&amp;#xE1;-Hlavat&amp;#xE1; L, Jezek J, Jezek P
    Oxidative stress of mitochondrial origin, i.e. elevated mitochondrial superoxide production, belongs to major factors determining aging and oxidative-stress-related diseases. Antioxidants, such as the mitochondria-targeted coenzyme Q, MitoQ(10), may prevent or cure these pathological conditions. To elucidate pro- and anti-oxidant action of MitoQ(10), we studied its effects on HepG2 cell respiration, mitochondrial network morphology, and rates of superoxide release (above that neutralized by superoxide dismutase) to the mitochondrial matrix (J(m)). MitoSOX Red fluorescence confocal microscopy monitoring of J(m) rates showed pro-oxidant effects of 3.5-fold increased J(m) with MitoQ(10). MitoQ(10) induced fission of the mitochondrial ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546986</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:39 +0100</pubDate>
            <guid isPermaLink="false">2546986</guid>        </item>
        <item>
            <title>Fibrocyte CXCR4 regulation as a therapeutic target in pulmonary fibrosis.</title>
            <link>http://www.medworm.com/index.php?rid=2546984&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433312%26dopt%3DAbstract</link>
            <description>Authors: Mehrad B, Burdick MD, Strieter RM
    Fibrotic interstitial lung diseases are characterized by progressive decline in lung function and premature death from respiratory failure. Fibrocytes are circulating bone marrow-derived progenitor cells that traffic to the lungs and contribute to fibrosis and may represent novel therapeutic targets in these diseases. We have previously found the recruitment of fibrocytes to the lung to be dependent on the chemokine ligand CXCL12. Given that the expression of the CXCL12 receptor, CXCR4, can be modulated pharmacologically in other cell types, we tested the hypotheses that the regulation of CXCR4 expression on fibrocytes mediates their influx to the lung in the context of pulmonary fibrosis and that pharmacologic inhibition of this process resul...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546984</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:36 +0100</pubDate>
            <guid isPermaLink="false">2546984</guid>        </item>
        <item>
            <title>NO-sensitive guanylyl cyclase beta1 subunit is peripherally associated to chromosomes during mitosis. Novel role in chromatin condensation and cell cycle progression.</title>
            <link>http://www.medworm.com/index.php?rid=2546981&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433313%26dopt%3DAbstract</link>
            <description>Authors: Pifarr&amp;#xE9; P, Baltrons MA, F&amp;#xF6;ldi I, Garc&amp;#xED;a A
    NO-sensitive guanylyl cyclase (GC(NO)), the major NO target, is involved in important regulatory functions in the cardiovascular, gastrointestinal and central nervous systems. GC(NO) exists as heterodimers of alpha(1/2) and beta1 subunits. Deletion of the obligate beta1 dimerizing partner abrogates NO/cGMP signaling and shortens the life span of KO mice. Localization studies in the CNS have shown that beta1 is more widespread than alpha subunits and in some areas is the only GC(NO) subunit expressed, suggesting that beta1 may have GC(NO)-independent functions. GC(NO) is predominantly cytosolic, but association to membranes and other intracellular structures has been described. Here, we show localization of beta1 in cytop...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546981</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:34 +0100</pubDate>
            <guid isPermaLink="false">2546981</guid>        </item>
        <item>
            <title>Suppression of urokinase plasminogen activator receptor inhibits proliferation and migration of pancreatic adenocarcinoma cells via regulation of ERK/p38 signaling.</title>
            <link>http://www.medworm.com/index.php?rid=2546978&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433314%26dopt%3DAbstract</link>
            <description>In this study, two different PDAC cell lines were used to examine the effect of small interfering (si) RNAs to uPAR, uPA and PAI-2 on proliferation, apoptosis, migration and MAP kinase activation. In both PDAC cell lines, siRNA to uPAR significantly inhibited cell proliferation and migration and stimulated apoptosis, to a greater extent than uPA siRNA. When either PDAC cell line was treated with uPAR siRNA, the level of phosphorylated ERK (p-ERK) decreased substantially, whereas phosphorylated p38 (p-p38) increased when compared to non-silencing control, uPA siRNA or PAI-2 siRNA treatment. This resulted in enhancement of the p-p38/p-ERK ratio which favors cancer cell arrest. Interestingly, uPAR protein expression was suppressed by p-ERK inhibition and stimulated with p-p38 inhibition, sugg...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546978</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:31 +0100</pubDate>
            <guid isPermaLink="false">2546978</guid>        </item>
        <item>
            <title>Bax inhibitor-1 overexpression reduces the suppressive effect of calcium mobilizing agent on adipogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2546975&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19433315%26dopt%3DAbstract</link>
            <description>Authors: Yu J, Kwon KB, Park JW, Chae HJ, Park BH
    Bax inhibitor-1 is a conserved protein which suppresses endoplasmic reticulum stress-induced apoptosis and regulates calcium release from the endoplasmic reticulum. Recent studies have revealed that adipogenesis, the process of adipocyte differentiation, is influenced by a change of intracellular calcium concentration. Here, we examined the effect of endoplasmic reticulum calcium regulation by Bax inhibitor-1 on adipogenesis using 3T3-L1 preadipocytes stably transfected with a pcDNA3-BI-1-HA plasmid. Bax inhibitor-1 functionality was confirmed by inhibiting the thapsigargin-induced increase of endoplasmic reticulum stress markers. Bax inhibitor-1 overexpression did not alter normal process of adipogenesis. Thapsigargin treatment inhibit...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546975</comments>
            <pubDate>Sun, 28 Jun 2009 04:02:29 +0100</pubDate>
            <guid isPermaLink="false">2546975</guid>        </item>
        <item>
            <title>&quot;What can mitochondrial heterogeneity tell us about mitochondrial dynamics and autophagy?&quot;</title>
            <link>http://www.medworm.com/index.php?rid=2546905&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19549572%26dopt%3DAbstract</link>
            <description>In conclusion, mitochondrial subcellular heterogeneity is a reflection of the mitochondrial lifecycle that involves frequent fusion events in which components may be unevenly mixed and followed by fission events generating disparate daughter mitochondria, some of which may fuse again, others will remain solitary and join a pre-autophagic pool.
    PMID: 19549572 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546905</comments>
            <pubDate>Fri, 19 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546905</guid>        </item>
        <item>
            <title>Mitochondria matter: new concepts of dynamics and roles in pathophysiology.</title>
            <link>http://www.medworm.com/index.php?rid=2546908&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19545643%26dopt%3DAbstract</link>
            <description>Authors: Kargul J, Laurent GJ
    
    PMID: 19545643 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546908</comments>
            <pubDate>Thu, 18 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546908</guid>        </item>
        <item>
            <title>The E2F family and the role of E2F1 in apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=2546910&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19539777%26dopt%3DAbstract</link>
            <description>Authors: Wu Z, Zheng S, Yu Q
    The E2F family of transcription factors plays a pivotal role in the regulation of cellular proliferation and differentiation. Although the deregulation of E2Fs is considered an oncogenic event that predisposes immortalized cells to transformation, paradoxically, E2F1 is also equipped with an ability to induce apoptosis under certain cellular contexts. It has become evident that E2Fs, in particular E2F1, participate in many aspects of the apoptotic process, either by acting alone or in cooperation with other factors, such as p53, to protect organisms from tumor development in the face of oncogenic lesions. Given the frequent inactivation of p53 in human cancers, the E2F1-induced apoptosis pathway is rapidly gaining attention as a key mechanism to compensate ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546910</comments>
            <pubDate>Mon, 15 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546910</guid>        </item>
        <item>
            <title>Resveratrol: cellular actions of a potent natural chemical that confers a diversity of health benefits.</title>
            <link>http://www.medworm.com/index.php?rid=2546912&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19527796%26dopt%3DAbstract</link>
            <description>Authors: Marques FZ, Markus MA, Morris BJ
    Resveratrol is a polyphenolic flavonoid with potent anti-oxidant activity. It is found in a diversity of plants, notably berry fruit, and is attracting increased attention due to its health benefits, especially in common age-related diseases such as cancer, type 2 diabetes, cardiovascular disease, and neurological conditions. Resveratrol has positive effects on metabolism and can increase the lifespan of various organisms. Its effects arise from its capacity to interact with multiple molecular targets involved in diverse intracellular pathways. Most well-known is the ability of resveratrol to activate sirtuins, a class of NAD(+)-dependent deacetylases that affect multiple transcription factors and other protein targets. More potent sirtuin acti...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546912</comments>
            <pubDate>Thu, 11 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546912</guid>        </item>
        <item>
            <title>The interaction of estrogen receptor alpha and caveolin-3 regulates connexin43 phosphorylation in metabolic inhibition-treated rat cardiomyocytes.</title>
            <link>http://www.medworm.com/index.php?rid=2546916&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19523531%26dopt%3DAbstract</link>
            <description>Authors: Chung TH, Wang SM, Liang JY, Yang SH, Wu JC
    Caveolin-3, the major caveolin isoform in cardiomyocytes, plays an important role in the rapid signaling pathways initiated by stimulation of the membrane-associated molecules. To examine the role of caveolin-3 in regulating estrogen receptor alpha in cardiomyocytes, we investigate whether the membrane estrogen receptor alpha associates with caveolin-3 and whether this association is linked to the 17beta-estradiol-mediated signals. In control cardiomyocytes, following discontinuous sucrose gradient centrifugation, caveolin-3 was found predominantly in the lipid raft buoyant fractions, whereas it was distributed to both the buoyant and non-lipid raft heavy fractions following metabolic inhibition treatment. Confocal microscopy showed ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546916</comments>
            <pubDate>Tue, 09 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546916</guid>        </item>
        <item>
            <title>Atherosclerotic plaque development.</title>
            <link>http://www.medworm.com/index.php?rid=2546914&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19523532%26dopt%3DAbstract</link>
            <description>Authors: Bui Q, Prempeh M, Wilensky RL
    Atherosclerosis is now recognized as an inflammatory/immunomodulatory reaction to the presence of oxidized low-density lipoproteins within the arterial wall, often times in the setting of such risk factors as family history, hypercholesterolemia, high blood pressure, diabetes mellitus and smoking. The progression to high-risk lesions such as thin-fibrous cap atheromas results in an increased risk of sudden death, acute myocardial infarction and ischemic stroke. The interplay of macrophages, T lymphocytes and mast cells play a central role in both the development but more importantly in the progression of coronary and carotid artery disease to high-risk phenotypes.
    PMID: 19523532 [PubMed - as supplied by publisher] (Source: The International Jo...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546914</comments>
            <pubDate>Tue, 09 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546914</guid>        </item>
        <item>
            <title>Editorial.</title>
            <link>http://www.medworm.com/index.php?rid=2546922&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19501184%26dopt%3DAbstract</link>
            <description>Authors: Rossignol R, Karbowski M
    
    PMID: 19501184 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546922</comments>
            <pubDate>Fri, 05 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546922</guid>        </item>
        <item>
            <title>Nucleostemin: A latecomer with new tricks.</title>
            <link>http://www.medworm.com/index.php?rid=2546920&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19501670%26dopt%3DAbstract</link>
            <description>Authors: Tsai RY, Meng L
    Nucleostemin was first identified in neural stem cells and has become a focus of research in cell cycle control, tumorigenesis and cellular senescence. As the biology of nucleostemin begins to be unveiled in multiple species, an ensuing task is to resolve the apparent differences between the functions of mammalian and invertebrate nucleostemin and its homologues, an issue of pressing interest given the role of nucleostemin in stem cell self-renewal and tissue regeneration. A genome-wide search reveals that nucleostemin and its closest homologue, GNL3L, only emerge as separate genes in vertebrates and possess conserved protein sequences as evolution proceeded to the Mammalia. The invertebrate orthologue of nucleostemin and GNL3L resembles GNL3L more than it does...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546920</comments>
            <pubDate>Fri, 05 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546920</guid>        </item>
        <item>
            <title>Pim-3 protects against cardiomyocyte apoptosis in anoxia/reoxygenation injury via p38-mediated signal pathway.</title>
            <link>http://www.medworm.com/index.php?rid=2546918&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19505587%26dopt%3DAbstract</link>
            <description>Authors: Liu D, He M, Yi B, Guo WH, Que AL, Zhang JX
    Although anoxic preconditioning (APC) in the myocardium has been investigated for many years, its physiological mechanism is still not completely understood. Increasing evidence indicates that transiently increased resistance to ischemic damage following APC is dependent on de novo proteins synthesis. However, the key effector pathway(s) associated with APC still remains unclear. The proto-oncogene Pim kinase belongs to a serine/threoine protein kinase family, consists of Pim-1, Pim-2 and Pim-3 and has been implicated in stimulating cell growth and inhibiting cell apoptosis. Therefore we assumed that Pim-3 expression might be aberrantly induced in cardiomyocytes that were subjected to anoxia/reoxygenation (A/R) injury and that Pim-3 ...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546918</comments>
            <pubDate>Fri, 05 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546918</guid>        </item>
        <item>
            <title>Cigarette smoke exposure causes changes in Scavenger Receptor B1 level and distribution in lung cells.</title>
            <link>http://www.medworm.com/index.php?rid=2546932&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19497383%26dopt%3DAbstract</link>
            <description>Authors: Valacchi G, Davis PA, Khan EM, Lanir R, Maioli E, Pecorelli A, Cross CE, Goldkorn T
    Scavenger Receptor B1 has been shown to play a prominent role in the uptake and delivery of vitamin E from HDL and is likely involved in regulating vitamin E in the lung. We have previously demonstrated that lung Scavenger Receptor B1 levels (protein and mRNA) are modulated by cigarette smoke in mice and this was accompanied by changes in lung vitamin E. To further characterize the molecular mechanism(s) involved in this process, human alveolar epitheliall cells were exposed to cigarette smoke and Scavenger Receptor B1 cellular levels and distribution were assessed. Results demonstrated that Scavenger Receptor B1 localizes in patches on the cellular membrane and in the perinuclear area of contr...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546932</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546932</guid>        </item>
        <item>
            <title>New ATPase regulators-p97 goes to the PUB.</title>
            <link>http://www.medworm.com/index.php?rid=2546930&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19497384%26dopt%3DAbstract</link>
            <description>Authors: Madsen L, Seeger M, Semple CA, Hartmann-Petersen R
    The conserved eukaryotic AAA-type ATPase complex, known as p97 or VCP in mammals and Cdc48 in yeast, is involved in a number of cellular pathways, including fusion of homotypic membranes, protein degradation, and activation of membrane-bound transcription factors. Most likely, p97 is directed to this broad spectrum of cellular functions through its binding to specific cofactors. More than 20 different p97 cofactors have been described to date and our understanding of their cellular functions is rapidly expanding. Common to these proteins is their intimate connection with the ubiquitin system. Recently, a small, conserved family of proteins, containing PUB domains, was found to function as p97 adaptors. Intriguingly, their asso...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546930</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546930</guid>        </item>
        <item>
            <title>Disruption of the blood-testis barrier integrity by bisphenol A in vitro: Is this a suitable model for studying blood-testis barrier dynamics?</title>
            <link>http://www.medworm.com/index.php?rid=2546928&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19497385%26dopt%3DAbstract</link>
            <description>In this study, it was shown that in adult rats treated with acute doses of bisphenol A, a small but statistically insignificant percentage of seminiferous tubules in the testes displayed signs of germ cell loss, consistent with some earlier reports. It also failed to disrupt the blood-testis barrier in vivo. This is possibly due to the low bioavailability of free bisphenol A in the systemic circulation. However, bisphenol A disrupted the blood-testis barrier when administered to immature 20-day-old rats, consistent with earlier reports concerning the higher susceptibility of immature rats towards bisphenol A. This observation was confirmed using primary Sertoli cells cultured in vitro with established tight junction-permeability barrier that mimicked the blood-testis barrier in vivo. The r...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546928</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546928</guid>        </item>
        <item>
            <title>MicroRNAs, ultraconserved genes and colorectal cancers.</title>
            <link>http://www.medworm.com/index.php?rid=2546926&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19497386%26dopt%3DAbstract</link>
            <description>Authors: Rossi S, Kopetz S, Davuluri R, Hamilton SR, Calin GA
    In this review we present some recent advances in understanding the roles of non-coding RNAs, including microRNAs and ultraconserved genes in colorectal cancer and the way these advances can be translated for better cure of patients. MicroRNAs are a class of small RNAs that do not code for proteins and yet function as gene regulators. The deregulation of microRNA expression is involved in the initiation, progression, and dissemination of any type of human tumor. The underlying mechanisms of microRNA deregulation in human cancers are just starting to be understood. Germline and somatic mutations in microRNAs or polymorphisms in the messenger protein-coding RNAs targeted by microRNAs may also contribute to the tumor phenotype....</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546926</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546926</guid>        </item>
        <item>
            <title>Is the inhibition of nicotinic acetylcholine receptors by bupropion involved in its clinical actions?</title>
            <link>http://www.medworm.com/index.php?rid=2546924&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19497387%26dopt%3DAbstract</link>
            <description>Authors: Arias HR
    In this mini review we will focus on those molecular and cellular mechanisms exerted by bupropion (BP), ultimately leading to the antidepressant and anti-nicotinic properties described for this molecule. The main pharmacological mechanism is based on the fact that BP induces the release as well as inhibits the reuptake of neurotransmitters such as a dopamine (DA) and norepinephrine (NE). Additional mechanisms of action have been also determined. For example, BP is a noncompetitive antagonist (NCA) of several nicotinic acetylcholine receptors (AChRs). Based on this evidence, the dual antidepressant and anti-nicotinic activity of BP is currently considered to be mediated by its stimulatory action on the DA and NE systems as well as its inhibitory action on AChRs. Consid...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546924</comments>
            <pubDate>Mon, 01 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2546924</guid>        </item>
        <item>
            <title>Ca(2+)-dependent regulation of mitochondrial dynamics by the Miro-Milton complex.</title>
            <link>http://www.medworm.com/index.php?rid=2546934&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19481172%26dopt%3DAbstract</link>
            <description>Authors: Liu X, Hajn&amp;#xF3;czky G
    Calcium oscillations control mitochondrial motility along the microtubules and in turn, support on-demand distribution of mitochondria. However, the mechanism mediating the Ca(2+) effect remained a mystery. Recently, several papers reported on the Ca(2+)-dependent regulation of mitochondrial dynamics by a Miro-Milton complex linking mitochondria to kinesin motors. Both mitochondrial motility and fusion-fission dynamics seem to be sensitive to a Ca(2+)-dependent switch by this complex. Evidence is emerging that calcium signaling through Miro-Milton is central to coordination of the local oxidative metabolism with the energy demands and protection against Ca(2+)-induced cell injury.
    PMID: 19481172 [PubMed - as supplied by publisher] (Source: The Inter...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546934</comments>
            <pubDate>Tue, 26 May 2009 23:00:00 +0100</pubDate>
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            <title>M-LDH physically associated with sarcolemmal K(ATP) channels mediates cytoprotection in heart embryonic H9C2 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2546942&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19464385%26dopt%3DAbstract</link>
            <description>Authors: Jovanovi&amp;#x107; S, Du Q, Sukhodub A, Jovanovi&amp;#x107; A
    Muscle form of lactate dehydrogenase (M-LDH) physically associate with K(ATP) channel subunits, Kir6.2 and SUR2A, and is an integral part of the ATP-sensitive K(+) (K(ATP)) channel protein complex in the heart. Here, we have shown that concomitant introduction of viral constructs containing truncated and mutated forms of M-LDH (DeltaM-LDH) and 193gly-M-LDH respectively, generate a phenotype of rat heart embryonic H9C2 cells that do not contain functional M-LDH as a part of the K(ATP) channel protein complex. The K(+) current was increased in wild type cells, but not in cells expressing DeltaM-LDH/193gly-M-LDH, when they were exposed to chemical hypoxia induced by 2,4 dinitrophenol (DNP; 10mM). At the same time, the outcome...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546942</comments>
            <pubDate>Wed, 20 May 2009 23:00:00 +0100</pubDate>
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        <item>
            <title>Mitochondrial functional complementation in mitochondrial DNA-based diseases.</title>
            <link>http://www.medworm.com/index.php?rid=2546940&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19464386%26dopt%3DAbstract</link>
            <description>Authors: Nakada K, Sato A, Hayashi JI
    Mitochondria exist in networks that are continuously remodeled through fusion and fission. Why do individual mitochondria in living cells fuse and divide continuously? Protein machinery and molecular mechanism for the dynamic nature of mitochondria have been almost clarified. However, the biological significance of the mitochondrial fusion and fission events has been poorly understood, although there is a possibility that mitochondrial fusion and fission are concerned with quality controls of mitochondria. trans-mitochondrial cell and mouse models possessing heteroplasmic populations of mitochondrial DNA (mtDNA) haplotypes are quite efficient for answering this question, and one of the answers is &quot;mitochondrial functional complementation&quot; that is a...</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546940</comments>
            <pubDate>Wed, 20 May 2009 23:00:00 +0100</pubDate>
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        <item>
            <title>Down-regulation of neprilysin (EC3.4.24.11) expression in vascular endothelial cells by laminar shear stress involves NADPH oxidase-dependent ROS production.</title>
            <link>http://www.medworm.com/index.php?rid=2546938&amp;cid=s_35635_60_f&amp;fid=35635&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19464387%26dopt%3DAbstract</link>
            <description>In conclusion, we confirm for the first time that NEP expression is down-regulated in vascular endothelial cells by physiological laminar shear, possibly via a mechanotransduction mechanism involving NADPH oxidase-induced ROS production.
    PMID: 19464387 [PubMed - as supplied by publisher] (Source: The International Journal of Biochemistry and Cell Biology)</description>
            <author>The International Journal of Biochemistry and Cell Biology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2546938</comments>
            <pubDate>Wed, 20 May 2009 23:00:00 +0100</pubDate>
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