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10.1074/jbc.M115.687129 http://scihub22266oqcxt.onion/10.1074/jbc.M115.687129 C4817176!4817176!26839314     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 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 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 294.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2016 ; 291 (14): 7450-64 Nephropedia Template TP {{tp|p=26839314|t=2016. Ubiquitin-specific Protease 20 Regulates the Reciprocal Functions of ?-Arrestin2 in Toll-like Receptor 4-promoted Nuclear Factor ?B (NF?B) Activation* |pdf=|usr=}}{{26839314}} gab.com Text Ubiquitin-specific Protease 20 Regulates the Reciprocal Functions of -Arrestin2 in Toll-like Receptor 4-promoted Nuclear Factor B (NF B) Activation* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=26839314 #FOAvip Toll-like receptor 4 (TLR4) promotes vascular inflammatory disorders such as neointimal hyperplasia and atherosclerosis. TLR4 triggers NF?B signaling through the ubiquitin ligase TRAF6 (tumor necrosis factor receptor-associated factor 6). TRAF6 activity can be impeded by deubiquitinating enzymes like ubiquitin-specific protease 20 (USP20), which can reverse TRAF6 autoubiquitination, and by association with the multifunctional adaptor protein ?-arrestin2. Although ?-arrestin2 effects on TRAF6 suggest an anti-inflammatory role, physiologic ?-arrestin2 promotes inflammation in atherosclerosis and neointimal hyperplasia. We hypothesized that anti- and proinflammatory dimensions of ?-arrestin2 activity could be dictated by ?-arrestin2's ubiquitination status, which has been linked with its ability to scaffold and localize activated ERK1/2 to signalosomes. With purified proteins and in intact cells, our protein interaction studies showed that TRAF6/USP20 association and subsequent USP20-mediated TRAF6 deubiquitination were ?-arrestin2-dependent. Generation of transgenic mice with smooth muscle cell-specific expression of either USP20 or its catalytically inactive mutant revealed anti-inflammatory effects of USP20 in vivo and in vitro. Carotid endothelial denudation showed that antagonizing smooth muscle cell USP20 activity increased NF?B activation and neointimal hyperplasia. We found that ?-arrestin2 ubiquitination was promoted by TLR4 and reversed by USP20. The association of USP20 with ?-arrestin2 was augmented when ?-arrestin2 ubiquitination was prevented and reduced when ?-arrestin2 ubiquitination was rendered constitutive. Constitutive ?-arrestin2 ubiquitination also augmented NF?B activation. We infer that pro- and anti-inflammatory activities of ?-arrestin2 are determined by ?-arrestin2 ubiquitination and that changes in USP20 expression and/or activity can therefore regulate inflammatory responses, at least in part, by defining the ubiquitination status of ?-arrestin2. Twit Text FOAVip Ubiquitin-specific Protease 20 Regulates the Reciprocal Functions of -Arrestin2 in Toll-like Receptor 4-promoted Nuclear Factor B (NF B) Activation* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=26839314 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26839314 #FOAvip English Wikipedia <ref>{{Cite pmid|26839314}}</ref> Ubiquitin-specific Protease 20 Regulates the Reciprocal Functions of ?-Arrestin2 in Toll-like Receptor 4-promoted Nuclear Factor ?B (NF?B) Activation* #MMPMID26839314 Jean-Charles PY; Zhang L; Wu JH; Han So; Brian L; Freedman NJ; Shenoy SK J Biol Chem 2016[Apr]; 291 (14): 7450-64 PMID26839314show ga Toll-like receptor 4 (TLR4) promotes vascular inflammatory disorders such as neointimal hyperplasia and atherosclerosis. TLR4 triggers NF?B signaling through the ubiquitin ligase TRAF6 (tumor necrosis factor receptor-associated factor 6). TRAF6 activity can be impeded by deubiquitinating enzymes like ubiquitin-specific protease 20 (USP20), which can reverse TRAF6 autoubiquitination, and by association with the multifunctional adaptor protein ?-arrestin2. Although ?-arrestin2 effects on TRAF6 suggest an anti-inflammatory role, physiologic ?-arrestin2 promotes inflammation in atherosclerosis and neointimal hyperplasia. We hypothesized that anti- and proinflammatory dimensions of ?-arrestin2 activity could be dictated by ?-arrestin2's ubiquitination status, which has been linked with its ability to scaffold and localize activated ERK1/2 to signalosomes. With purified proteins and in intact cells, our protein interaction studies showed that TRAF6/USP20 association and subsequent USP20-mediated TRAF6 deubiquitination were ?-arrestin2-dependent. Generation of transgenic mice with smooth muscle cell-specific expression of either USP20 or its catalytically inactive mutant revealed anti-inflammatory effects of USP20 in vivo and in vitro. Carotid endothelial denudation showed that antagonizing smooth muscle cell USP20 activity increased NF?B activation and neointimal hyperplasia. We found that ?-arrestin2 ubiquitination was promoted by TLR4 and reversed by USP20. The association of USP20 with ?-arrestin2 was augmented when ?-arrestin2 ubiquitination was prevented and reduced when ?-arrestin2 ubiquitination was rendered constitutive. Constitutive ?-arrestin2 ubiquitination also augmented NF?B activation. We infer that pro- and anti-inflammatory activities of ?-arrestin2 are determined by ?-arrestin2 ubiquitination and that changes in USP20 expression and/or activity can therefore regulate inflammatory responses, at least in part, by defining the ubiquitination status of ?-arrestin2. äUbiquitin-specific Protease 20 Regulates the Reciprocal Functions of ?(epmc).pdf DeepDyve Pubget Overpricing