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10.1016/j.tcb.2015.06.002 http://scihub22266oqcxt.onion/10.1016/j.tcb.2015.06.002 C4734635!4734635!26159692     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26159692&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26159692.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Trends+Cell+Biol 2015 ; 25 (9): 545-55 Nephropedia Template TP {{tp|p=26159692|t=2015. Regulation of mTORC1 by PI3K Signaling |pdf=|usr=}}{{26159692}} gab.com Text Regulation of mTORC1 by PI3K Signaling JO: Trends Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26159692 #FOAvip The class I phosphoinositide 3-kinase (PI3K) - mechanistic target of rapamycin complex 1 (mTORC1) signaling network directs cellular metabolism and growth. Activation of mTORC1, which is composed of mTOR, Raptor, mLST8, PRAS40, and DEPTOR, depends on the Rag and Rheb GTPases, and requires signals from amino acids, glucose, oxygen, energy (ATP), and growth factors (including cytokines and hormones such as insulin). Here we discuss the signal transduction mechanisms through which growth factor-responsive PI3K signaling activates mTORC1. We focus on how PI3K-dependent activation of Akt and spatial regulation of the TSC complex (composed of TSC1, TSC2, and TBC1D7) switches on Rheb at the lysosome, where mTORC1 is activated. Integration of PI3K- and amino acid-dependent signals upstream of mTORC1 at the lysosome is detailed in a working model. A coherent understanding of the PI3K-mTORC1 network is imperative as its dysregulation has been implicated in diverse pathologies including cancer, diabetes, autism, and aging. Twit Text FOAVip Regulation of mTORC1 by PI3K Signaling ????Trends Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26159692 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26159692 #FOAvip English Wikipedia <ref>{{Cite pmid|26159692}}</ref> Regulation of mTORC1 by PI3K Signaling #MMPMID26159692 Dibble CC; Cantley LC Trends Cell Biol 2015[Sep]; 25 (9): 545-55 PMID26159692show ga The class I phosphoinositide 3-kinase (PI3K) - mechanistic target of rapamycin complex 1 (mTORC1) signaling network directs cellular metabolism and growth. Activation of mTORC1, which is composed of mTOR, Raptor, mLST8, PRAS40, and DEPTOR, depends on the Rag and Rheb GTPases, and requires signals from amino acids, glucose, oxygen, energy (ATP), and growth factors (including cytokines and hormones such as insulin). Here we discuss the signal transduction mechanisms through which growth factor-responsive PI3K signaling activates mTORC1. We focus on how PI3K-dependent activation of Akt and spatial regulation of the TSC complex (composed of TSC1, TSC2, and TBC1D7) switches on Rheb at the lysosome, where mTORC1 is activated. Integration of PI3K- and amino acid-dependent signals upstream of mTORC1 at the lysosome is detailed in a working model. A coherent understanding of the PI3K-mTORC1 network is imperative as its dysregulation has been implicated in diverse pathologies including cancer, diabetes, autism, and aging. äRegulation of mTORC1 by PI3K Signaling (epmc).pdf DeepDyve Pubget Overpricing