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10.1016/j.cell.2013.04.048 http://scihub22266oqcxt.onion/10.1016/j.cell.2013.04.048 C3681429!3681429!23746844     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2013 ; 153 (6): 1327-39 Nephropedia Template TP {{tp|p=23746844|t=2013. HIF1A employs CDK8-Mediator to stimulate RNAPII elongation |pdf=|usr=}}{{23746844}} gab.com Text HIF1A employs CDK8-Mediator to stimulate RNAPII elongation JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=23746844 #FOAvip The transcription factor HIF1A is a key mediator of the cellular response to hypoxia. Despite the importance of HIF1A in homeostasis and various pathologies, little is known about how it regulates RNA polymerase II (RNAPII). We report here that HIF1A employs a specific variant of the Mediator complex to stimulate RNAPII elongation. The Mediator-associated kinase CDK8, but not the paralog CDK19, is required for induction of many HIF1A target genes. HIF1A induces binding of CDK8-Mediator and the Super Elongation Complex (SEC), containing AFF4 and CDK9, to alleviate RNAPII pausing. CDK8 is dispensable for HIF1A chromatin binding and histone acetylation, but it is essential for binding of SEC and RNAPII elongation. Global analysis of active RNAPII reveals that hypoxia-inducible genes are paused and active prior to their induction. Our results provide a mechanistic link between HIF1A and CDK8, two potent oncogenes, in the cellular response to hypoxia. Twit Text FOAVip HIF1A employs CDK8-Mediator to stimulate RNAPII elongation ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=23746844 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23746844 #FOAvip English Wikipedia <ref>{{Cite pmid|23746844}}</ref> HIF1A employs CDK8-Mediator to stimulate RNAPII elongation #MMPMID23746844 Galbraith MD; Allen MA; Bensard CL; Wang X; Schwinn MK; Qin B; Long HW; Daniels DL; Hahn WC; Dowell RD; Espinosa JM Cell 2013[Jun]; 153 (6): 1327-39 PMID23746844show ga The transcription factor HIF1A is a key mediator of the cellular response to hypoxia. Despite the importance of HIF1A in homeostasis and various pathologies, little is known about how it regulates RNA polymerase II (RNAPII). We report here that HIF1A employs a specific variant of the Mediator complex to stimulate RNAPII elongation. The Mediator-associated kinase CDK8, but not the paralog CDK19, is required for induction of many HIF1A target genes. HIF1A induces binding of CDK8-Mediator and the Super Elongation Complex (SEC), containing AFF4 and CDK9, to alleviate RNAPII pausing. CDK8 is dispensable for HIF1A chromatin binding and histone acetylation, but it is essential for binding of SEC and RNAPII elongation. Global analysis of active RNAPII reveals that hypoxia-inducible genes are paused and active prior to their induction. Our results provide a mechanistic link between HIF1A and CDK8, two potent oncogenes, in the cellular response to hypoxia. äHIF1A employs CDK8-Mediator to stimulate RNAPII elongation (epmc).pdf DeepDyve Pubget Overpricing