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10.1038/s41420-018-0056-3 http://scihub22266oqcxt.onion/10.1038/s41420-018-0056-3 C5955943!5955943!29796309     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Discov 2018 ; 4 (ä): ä Nephropedia Template TP {{tp|p=29796309|t=2018. Deubiquitinase function of A20 maintains and repairs endothelial barrier after lung vascular injury |pdf=|usr=}}{{29796309}} gab.com Text Deubiquitinase function of A20 maintains and repairs endothelial barrier after lung vascular injury JO: Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=29796309 #FOAvip Vascular endothelial cadherin (VE-cad) expression at endothelial adherens junctions (AJs) regulates vascular homeostasis. Here we show that endothelial A20 is required for VE-cad expression at AJs to maintain and repair the injured endothelial barrier. In endothelial cell (EC)-restricted Tnfaip3 (A20) knockout (A20?EC) mice, LPS challenge caused uncontrolled lung vascular leak and persistent sequestration of polymorphonuclear neutrophil (PMNs). Importantly, A20?EC mice exhibited drastically reduced VE-cad expression in lungs compared with wild-type counterparts. Endothelial expression of wild-type A20 but not the deubiquitinase-inactive A20 mutant (A20C103A) prevented VE-cad ubiquitination, restored VE-cad expression, and suppressed lung vascular leak in A20?EC mice. Interestingly, IRAK-M-mediated nuclear factor-?B (NF-?B) signaling downstream of TLR4 was required for A20 expression in ECs. interleukin-1 receptor-associated kinase M (IRAK-M) knockdown suppressed basal and LPS-induced A20 expression in ECs. Further, in vivo silencing of IRAK-M in mouse lung vascular ECs through the CRISPR-Cas9 system prevented expression of A20 and VE-cad while augmenting lung vascular leak. These results suggest that targeting of endothelial A20 is a potential therapeutic strategy to restore endothelial barrier integrity in the setting of acute lung injury. Twit Text FOAVip Deubiquitinase function of A20 maintains and repairs endothelial barrier after lung vascular injury ????Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=29796309 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29796309 #FOAvip English Wikipedia <ref>{{Cite pmid|29796309}}</ref> Deubiquitinase function of A20 maintains and repairs endothelial barrier after lung vascular injury #MMPMID29796309 Soni D; Wang DM; Regmi SC; Mittal M; Vogel SM; Schlüter D; Tiruppathi C Cell Death Discov 2018[]; 4 (ä): ä PMID29796309show ga Vascular endothelial cadherin (VE-cad) expression at endothelial adherens junctions (AJs) regulates vascular homeostasis. Here we show that endothelial A20 is required for VE-cad expression at AJs to maintain and repair the injured endothelial barrier. In endothelial cell (EC)-restricted Tnfaip3 (A20) knockout (A20?EC) mice, LPS challenge caused uncontrolled lung vascular leak and persistent sequestration of polymorphonuclear neutrophil (PMNs). Importantly, A20?EC mice exhibited drastically reduced VE-cad expression in lungs compared with wild-type counterparts. Endothelial expression of wild-type A20 but not the deubiquitinase-inactive A20 mutant (A20C103A) prevented VE-cad ubiquitination, restored VE-cad expression, and suppressed lung vascular leak in A20?EC mice. Interestingly, IRAK-M-mediated nuclear factor-?B (NF-?B) signaling downstream of TLR4 was required for A20 expression in ECs. interleukin-1 receptor-associated kinase M (IRAK-M) knockdown suppressed basal and LPS-induced A20 expression in ECs. Further, in vivo silencing of IRAK-M in mouse lung vascular ECs through the CRISPR-Cas9 system prevented expression of A20 and VE-cad while augmenting lung vascular leak. These results suggest that targeting of endothelial A20 is a potential therapeutic strategy to restore endothelial barrier integrity in the setting of acute lung injury. äDeubiquitinase function of A20 maintains and repairs endothelial barri(epmc).pdf DeepDyve Pubget Overpricing