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10.1038/ni.2981 http://scihub22266oqcxt.onion/10.1038/ni.2981 C4190666!4190666!25151490     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       Nat+Immunol 2014 ; 15 (10): 965-72 Nephropedia Template TP {{tp|p=25151490|t=2014. AMPK-TAB1 activated p38 drives human T cell senescence |pdf=|usr=}}{{25151490}} gab.com Text AMPK-TAB1 activated p38 drives human T cell senescence JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25151490 #FOAvip In T lymphocytes, p38 MAP kinase (MAPK) regulates pleiotropic functions and is activated by canonical MAPK signaling or the alternative T cell receptor (TCR) activation pathway. Here we show that senescent human T cells lack the canonical and alternative pathways of p38 activation, but spontaneously engage the metabolic master regulator AMPK to trigger p38 recruitment to the scaffold TAB1 causing p38 auto-phosphorylation. Signaling via this pathway inhibits telomerase activity, T cell proliferation and expression of key components of the TCR signalosome. Our findings identify an unrecognized mode of p38 activation in T cells driven by intracellular changes such as low-nutrient and DNA-damage signaling (?intra-sensory? pathway). The proliferative defect of senescent T cells is reversed by blocking AMPK-TAB1-dependent p38 activation. Twit Text FOAVip AMPK-TAB1 activated p38 drives human T cell senescence ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25151490 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25151490 #FOAvip English Wikipedia <ref>{{Cite pmid|25151490}}</ref> AMPK-TAB1 activated p38 drives human T cell senescence #MMPMID25151490 Lanna A; Henson SM; Escors D; Akbar AN Nat Immunol 2014[Oct]; 15 (10): 965-72 PMID25151490show ga In T lymphocytes, p38 MAP kinase (MAPK) regulates pleiotropic functions and is activated by canonical MAPK signaling or the alternative T cell receptor (TCR) activation pathway. Here we show that senescent human T cells lack the canonical and alternative pathways of p38 activation, but spontaneously engage the metabolic master regulator AMPK to trigger p38 recruitment to the scaffold TAB1 causing p38 auto-phosphorylation. Signaling via this pathway inhibits telomerase activity, T cell proliferation and expression of key components of the TCR signalosome. Our findings identify an unrecognized mode of p38 activation in T cells driven by intracellular changes such as low-nutrient and DNA-damage signaling (?intra-sensory? pathway). The proliferative defect of senescent T cells is reversed by blocking AMPK-TAB1-dependent p38 activation. äAMPK-TAB1 activated p38 drives human T cell senescence (epmc).pdf DeepDyve Pubget Overpricing