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10.1038/ncomms10477 http://scihub22266oqcxt.onion/10.1038/ncomms10477 C5476828!5476828!26795633     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=26795633|t=2016. p38? and ? promote heart hypertrophy by targeting the mTOR-inhibitory protein DEPTOR for degradation |pdf=|usr=}}{{26795633}} gab.com Text p38 and promote heart hypertrophy by targeting the mTOR-inhibitory protein DEPTOR for degradation JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26795633 #FOAvip Disrupted organ growth leads to disease development. Hypertrophy underlies postnatal heart growth and is triggered after stress, but the molecular mechanisms involved in these processes are largely unknown. Here we show that cardiac activation of p38? and p38? increases during postnatal development and by hypertrophy-inducing stimuli. p38?/? promote cardiac hypertrophy by phosphorylating the mTORC1 and mTORC2 inhibitor DEPTOR, which leads to its degradation and mTOR activation. Hearts from mice lacking one or both kinases are below normal size, have high levels of DEPTOR, low activity of the mTOR pathway and reduced protein synthesis. The phenotype of p38?/??/? mice is reverted by overactivation of mTOR with amino acids, shRNA-mediated knockdown of Deptor, or cardiomyocyte overexpression of active p38? and p38?. Moreover, in WT mice, heart weight is reduced by cardiac overexpression of DEPTOR. Our results demonstrate that p38?/? control heart growth by modulating mTOR pathway through DEPTOR phosphorylation and subsequent degradation. Twit Text FOAVip p38 and promote heart hypertrophy by targeting the mTOR-inhibitory protein DEPTOR for degradation ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26795633 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26795633 #FOAvip English Wikipedia <ref>{{Cite pmid|26795633}}</ref> p38? and ? promote heart hypertrophy by targeting the mTOR-inhibitory protein DEPTOR for degradation #MMPMID26795633 González-Terán B; López JA; Rodríguez E; Leiva L; Martínez-Martínez S; Bernal JA; Jiménez-Borreguero LJ; Redondo JM; Vazquez J; Sabio G Nat Commun 2016[]; 7 (ä): ä PMID26795633show ga Disrupted organ growth leads to disease development. Hypertrophy underlies postnatal heart growth and is triggered after stress, but the molecular mechanisms involved in these processes are largely unknown. Here we show that cardiac activation of p38? and p38? increases during postnatal development and by hypertrophy-inducing stimuli. p38?/? promote cardiac hypertrophy by phosphorylating the mTORC1 and mTORC2 inhibitor DEPTOR, which leads to its degradation and mTOR activation. Hearts from mice lacking one or both kinases are below normal size, have high levels of DEPTOR, low activity of the mTOR pathway and reduced protein synthesis. The phenotype of p38?/??/? mice is reverted by overactivation of mTOR with amino acids, shRNA-mediated knockdown of Deptor, or cardiomyocyte overexpression of active p38? and p38?. Moreover, in WT mice, heart weight is reduced by cardiac overexpression of DEPTOR. Our results demonstrate that p38?/? control heart growth by modulating mTOR pathway through DEPTOR phosphorylation and subsequent degradation. äp38? and ? promote heart hypertrophy by targeting the mTOR-inhibitory (epmc).pdf DeepDyve Pubget Overpricing