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10.1016/j.cell.2013.12.035 http://scihub22266oqcxt.onion/10.1016/j.cell.2013.12.035 C4384661!4384661!24440334     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2014 ; 156 (3): 563-76 Nephropedia Template TP {{tp|p=24440334|t=2014. Redox modification of nuclear actin by MICAL-2 regulates SRF signaling |pdf=|usr=}}{{24440334}} gab.com Text Redox modification of nuclear actin by MICAL-2 regulates SRF signaling JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=24440334 #FOAvip The serum response factor (SRF) binds to coactivators, such as myocardin-related transcription factor-A (MRTF-A), and mediates gene transcription elicited by diverse signaling pathways. SRF/MRTF-A-dependent gene transcription is activated when nuclear MRTF-A levels increase, enabling the formation of transcriptionally active SRF/MRTF-A complexes. The level of nuclear MRTF-A is regulated by nuclear G-actin, which binds to MRTF-A and promotes its nuclear export. However, pathways that regulate nuclear actin levels are poorly understood. Here we show that MICAL-2, an atypical actin-regulatory protein, mediates SRF/MRTF-A-dependent gene transcription elicited by nerve growth factor and serum. MICAL-2 induces redox-dependent depolymerization of nuclear actin, which decreases nuclear G-actin and increases MRTF-A in the nucleus. Furthermore, we show that MICAL-2 is a target of CCG-1423, a small molecule inhibitor of SRF/MRTF-A-dependent transcription that exhibits efficacy in various preclinical disease models. These data identify redox modification of nuclear actin as a regulatory switch that mediates SRF/MRTF-A-dependent gene transcription. Twit Text FOAVip Redox modification of nuclear actin by MICAL-2 regulates SRF signaling ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=24440334 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24440334 #FOAvip English Wikipedia <ref>{{Cite pmid|24440334}}</ref> Redox modification of nuclear actin by MICAL-2 regulates SRF signaling #MMPMID24440334 Lundquist MR; Storaska AJ; Liu TC; Larsen SD; Evans T; Neubig RR; Jaffrey SR Cell 2014[Jan]; 156 (3): 563-76 PMID24440334show ga The serum response factor (SRF) binds to coactivators, such as myocardin-related transcription factor-A (MRTF-A), and mediates gene transcription elicited by diverse signaling pathways. SRF/MRTF-A-dependent gene transcription is activated when nuclear MRTF-A levels increase, enabling the formation of transcriptionally active SRF/MRTF-A complexes. The level of nuclear MRTF-A is regulated by nuclear G-actin, which binds to MRTF-A and promotes its nuclear export. However, pathways that regulate nuclear actin levels are poorly understood. Here we show that MICAL-2, an atypical actin-regulatory protein, mediates SRF/MRTF-A-dependent gene transcription elicited by nerve growth factor and serum. MICAL-2 induces redox-dependent depolymerization of nuclear actin, which decreases nuclear G-actin and increases MRTF-A in the nucleus. Furthermore, we show that MICAL-2 is a target of CCG-1423, a small molecule inhibitor of SRF/MRTF-A-dependent transcription that exhibits efficacy in various preclinical disease models. These data identify redox modification of nuclear actin as a regulatory switch that mediates SRF/MRTF-A-dependent gene transcription. äRedox modification of nuclear actin by MICAL-2 regulates SRF signaling(epmc).pdf DeepDyve Pubget Overpricing