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10.15252/embj.201387725 http://scihub22266oqcxt.onion/10.15252/embj.201387725 C4339124!4339124!25535246     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25535246.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       EMBO+J 2015 ; 34 (3): 393-409 Nephropedia Template TP {{tp|p=25535246|t=2015. A THEMIS:SHP1 complex promotes T-cell survival |pdf=|usr=}}{{25535246}} gab.com Text A THEMIS:SHP1 complex promotes T-cell survival JO: EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=25535246 #FOAvip THEMIS is critical for conventional T-cell development, but its precise molecular function remains elusive. Here, we show that THEMIS constitutively associates with the phosphatases SHP1 and SHP2. This complex requires the adapter GRB2, which bridges SHP to THEMIS in a Tyr-phosphorylation-independent fashion. Rather, SHP1 and THEMIS engage with the N-SH3 and C-SH3 domains of GRB2, respectively, a configuration that allows GRB2-SH2 to recruit the complex onto LAT. Consistent with THEMIS-mediated recruitment of SHP to the TCR signalosome, THEMIS knock-down increased TCR-induced CD3-? phosphorylation, Erk activation and CD69 expression, but not LCK phosphorylation. This generalized TCR signalling increase led to augmented apoptosis, a phenotype mirrored by SHP1 knock-down. Remarkably, a KI mutation of LCK Ser59, previously suggested to be key in ERK-mediated resistance towards SHP1 negative feedback, did not affect TCR signalling nor ligand discrimination in vivo. Thus, the THEMIS:SHP complex dampens early TCR signalling by a previously unknown molecular mechanism that favours T-cell survival. We discuss possible implications of this mechanism in modulating TCR output signals towards conventional T-cell development and differentiation. Twit Text FOAVip A THEMIS:SHP1 complex promotes T-cell survival ????EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=25535246 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25535246 #FOAvip English Wikipedia <ref>{{Cite pmid|25535246}}</ref> A THEMIS:SHP1 complex promotes T-cell survival #MMPMID25535246 Paster W; Bruger AM; Katsch K; Grégoire C; Roncagalli R; Fu G; Gascoigne NR; Nika K; Cohnen A; Feller SM; Simister PC; Molder KC; Cordoba SP; Dushek O; Malissen B; Acuto O EMBO J 2015[Feb]; 34 (3): 393-409 PMID25535246show ga THEMIS is critical for conventional T-cell development, but its precise molecular function remains elusive. Here, we show that THEMIS constitutively associates with the phosphatases SHP1 and SHP2. This complex requires the adapter GRB2, which bridges SHP to THEMIS in a Tyr-phosphorylation-independent fashion. Rather, SHP1 and THEMIS engage with the N-SH3 and C-SH3 domains of GRB2, respectively, a configuration that allows GRB2-SH2 to recruit the complex onto LAT. Consistent with THEMIS-mediated recruitment of SHP to the TCR signalosome, THEMIS knock-down increased TCR-induced CD3-? phosphorylation, Erk activation and CD69 expression, but not LCK phosphorylation. This generalized TCR signalling increase led to augmented apoptosis, a phenotype mirrored by SHP1 knock-down. Remarkably, a KI mutation of LCK Ser59, previously suggested to be key in ERK-mediated resistance towards SHP1 negative feedback, did not affect TCR signalling nor ligand discrimination in vivo. Thus, the THEMIS:SHP complex dampens early TCR signalling by a previously unknown molecular mechanism that favours T-cell survival. We discuss possible implications of this mechanism in modulating TCR output signals towards conventional T-cell development and differentiation. äA THEMIS:SHP1 complex promotes T-cell survival (epmc).pdf DeepDyve Pubget Overpricing