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10.1016/j.jbc.2021.100687 http://scihub22266oqcxt.onion/10.1016/j.jbc.2021.100687 33891947!8141881!33891947     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2021 ; 296 (ä): 100687 Nephropedia Template TP {{tp|p=33891947|t=2021. Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era |pdf=|usr=}}{{33891947}} gab.com Text Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=33891947 #FOAvip Glucocorticoids are potent anti-inflammatory drugs that are used to treat an extraordinary range of human disease, including COVID-19, underscoring the ongoing importance of understanding their molecular mechanisms. Early studies of GR signaling led to broad acceptance of models in which glucocorticoid receptor (GR) monomers tether repressively to inflammatory transcription factors, thus abrogating inflammatory gene expression. However, newer data challenge this core concept and present an exciting opportunity to reframe our understanding of GR signaling. Here, we present an alternate, two-part model for transcriptional repression by glucocorticoids. First, widespread GR-mediated induction of transcription results in rapid, primary repression of inflammatory gene transcription and associated enhancers through competition-based mechanisms. Second, a subset of GR-induced genes, including targets that are regulated in coordination with inflammatory transcription factors such as NF-kappaB, exerts secondary repressive effects on inflammatory gene expression. Within this framework, emerging data indicate that the gene set regulated through the cooperative convergence of GR and NF-kappaB signaling is central to the broad clinical effectiveness of glucocorticoids in terminating inflammation and promoting tissue repair. Twit Text FOAVip Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=33891947 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33891947 #FOAvip English Wikipedia <ref>{{Cite pmid|33891947}}</ref> Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era #MMPMID33891947 Gerber AN; Newton R; Sasse SK J Biol Chem 2021[Jan]; 296 (ä): 100687 PMID33891947show ga Glucocorticoids are potent anti-inflammatory drugs that are used to treat an extraordinary range of human disease, including COVID-19, underscoring the ongoing importance of understanding their molecular mechanisms. Early studies of GR signaling led to broad acceptance of models in which glucocorticoid receptor (GR) monomers tether repressively to inflammatory transcription factors, thus abrogating inflammatory gene expression. However, newer data challenge this core concept and present an exciting opportunity to reframe our understanding of GR signaling. Here, we present an alternate, two-part model for transcriptional repression by glucocorticoids. First, widespread GR-mediated induction of transcription results in rapid, primary repression of inflammatory gene transcription and associated enhancers through competition-based mechanisms. Second, a subset of GR-induced genes, including targets that are regulated in coordination with inflammatory transcription factors such as NF-kappaB, exerts secondary repressive effects on inflammatory gene expression. Within this framework, emerging data indicate that the gene set regulated through the cooperative convergence of GR and NF-kappaB signaling is central to the broad clinical effectiveness of glucocorticoids in terminating inflammation and promoting tissue repair. |*COVID-19 Drug Treatment[MESH] |Animals[MESH] |Anti-Inflammatory Agents/*therapeutic use[MESH] |COVID-19/immunology/pathology/virology[MESH] |Dexamethasone/*therapeutic use[MESH] |Gene Expression Regulation[MESH] |Genomics/methods[MESH] |Glucocorticoids/*therapeutic use[MESH] |Humans[MESH] |Inflammation/prevention & control[MESH] |Models, Genetic[MESH] |NF-kappa B/antagonists & inhibitors/*genetics/immunology[MESH] |Receptors, Glucocorticoid/agonists/*genetics/immunology[MESH] |SARS-CoV-2/growth & development/immunology/pathogenicity[MESH] |Signal Transduction[MESH]Repression of transcription by the glucocorticoid receptor: A parsimon(epmc).pdf DeepDyve Pubget Overpricing