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10.1128/MCB.00645-15 http://scihub22266oqcxt.onion/10.1128/MCB.00645-15 C4648813!4648813 !26438598     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26438598 &cmd=llinks): Failed to open stream: HTTP request failed! 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Posttranscriptional Regulation of the Inflammatory Marker C-Reactive Protein by the RNA-Binding Protein HuR and MicroRNA 637 |pdf=|usr=}}{{26438598 }} gab.com Text Posttranscriptional Regulation of the Inflammatory Marker C-Reactive Protein by the RNA-Binding Protein HuR and MicroRNA 637 JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26438598 #FOAvip C-reactive protein (CRP), an acute-phase plasma protein, is a major component of inflammatory reactions functioning as a mediator of innate immunity. It has been widely used as a validated clinical biomarker of the inflammatory state in trauma, infection, and age-associated chronic diseases, including cancer and cardiovascular disease (CVD). Despite this, the molecular mechanisms that regulate CRP expression are not well understood. Given that the CRP 3' untranslated region (UTR) is long and AU rich, we hypothesized that CRP may be regulated posttranscriptionally by RNA-binding proteins (RBPs) and by microRNAs. Here, we found that the RBP HuR bound directly to the CRP 3' UTR and affected CRP mRNA levels. Through this interaction, HuR selectively increased CRP mRNA stability and promoted CRP translation. Interestingly, treatment with the age-associated inflammatory cytokine interleukin-6 (IL-6) increased binding of HuR to CRP mRNA, and conversely, HuR was required for IL-6-mediated upregulation of CRP expression. In addition, we identified microRNA 637 (miR-637) as a microRNA that potently inhibited CRP expression in competition with HuR. Taken together, we have uncovered an important posttranscriptional mechanism that modulates the expression of the inflammatory marker CRP, which may be utilized in the development of treatments for inflammatory processes that cause CVD and age-related diseases. Twit Text FOAVip Posttranscriptional Regulation of the Inflammatory Marker C-Reactive Protein by the RNA-Binding Protein HuR and MicroRNA 637 ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26438598 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26438598 #FOAvip English Wikipedia <ref>{{Cite pmid|26438598 }}</ref> Posttranscriptional Regulation of the Inflammatory Marker C-Reactive Protein by the RNA-Binding Protein HuR and MicroRNA 637 #MMPMID26438598 Kim Y ; Noren Hooten N ; Dluzen DF ; Martindale JL ; Gorospe M ; Evans MK Mol Cell Biol 2015[Dec]; 35 (24 ): 4212-21 PMID26438598 show ga C-reactive protein (CRP), an acute-phase plasma protein, is a major component of inflammatory reactions functioning as a mediator of innate immunity. It has been widely used as a validated clinical biomarker of the inflammatory state in trauma, infection, and age-associated chronic diseases, including cancer and cardiovascular disease (CVD). Despite this, the molecular mechanisms that regulate CRP expression are not well understood. Given that the CRP 3' untranslated region (UTR) is long and AU rich, we hypothesized that CRP may be regulated posttranscriptionally by RNA-binding proteins (RBPs) and by microRNAs. Here, we found that the RBP HuR bound directly to the CRP 3' UTR and affected CRP mRNA levels. Through this interaction, HuR selectively increased CRP mRNA stability and promoted CRP translation. Interestingly, treatment with the age-associated inflammatory cytokine interleukin-6 (IL-6) increased binding of HuR to CRP mRNA, and conversely, HuR was required for IL-6-mediated upregulation of CRP expression. In addition, we identified microRNA 637 (miR-637) as a microRNA that potently inhibited CRP expression in competition with HuR. Taken together, we have uncovered an important posttranscriptional mechanism that modulates the expression of the inflammatory marker CRP, which may be utilized in the development of treatments for inflammatory processes that cause CVD and age-related diseases. |3' Untranslated Regions/genetics [MESH] |Biomarkers/blood/metabolism [MESH] |C-Reactive Protein/*genetics/metabolism [MESH] |Cell Line, Tumor [MESH] |ELAV-Like Protein 1/blood/genetics/*metabolism [MESH] |Gene Expression Regulation, Neoplastic [MESH] |HeLa Cells [MESH] |Hep G2 Cells [MESH] |Humans [MESH] |Inflammation/genetics/immunology [MESH] |Interleukin-6/biosynthesis/genetics [MESH] |MicroRNAs/blood/*genetics [MESH] |RNA Interference [MESH] |RNA Processing, Post-Transcriptional/*genetics [MESH] |RNA, Messenger/genetics/*metabolism [MESH] |RNA, Small Interfering [MESH]Posttranscriptional Regulation of the Inflammatory Marker C-Reactive P(epmc).pdf DeepDyve Pubget Overpricing