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10.1016/j.molcel.2015.05.010 http://scihub22266oqcxt.onion/10.1016/j.molcel.2015.05.010 C4476372!4476372 !26051179     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26051179 &cmd=llinks): Failed to open stream: HTTP request failed! 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Skp2-Mediated RagA Ubiquitination Elicits a Negative Feedback to Prevent Amino-Acid-Dependent mTORC1 Hyperactivation by Recruiting GATOR1 |pdf=|usr=}}{{26051179 }} gab.com Text Skp2-Mediated RagA Ubiquitination Elicits a Negative Feedback to Prevent Amino-Acid-Dependent mTORC1 Hyperactivation by Recruiting GATOR1 JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=26051179 #FOAvip The regulation of RagA(GTP) is important for amino-acid-induced mTORC1 activation. Although GATOR1 complex has been identified as a negative regulator for mTORC1 by hydrolyzing RagA(GTP), how GATOR1 is recruited to RagA to attenuate mTORC1 signaling remains unclear. Moreover, how mTORC1 signaling is terminated upon amino acid stimulation is also unknown. We show that the recruitment of GATOR1 to RagA is induced by amino acids in an mTORC1-dependent manner. Skp2 E3 ligase drives K63-linked ubiquitination of RagA, which facilitates GATOR1 recruitment and RagA(GTP) hydrolysis, thereby providing a negative feedback loop to attenuate mTORC1 lysosomal recruitment and prevent mTORC1 hyperactivation. We further demonstrate that Skp2 promotes autophagy but inhibits cell size and cilia growth through RagA ubiquitination and mTORC1 inhibition. We thereby propose a negative feedback whereby Skp2-mediated RagA ubiquitination recruits GATOR1 to restrict mTORC1 signaling upon sustained amino acid stimulation, which serves a critical mechanism to maintain proper cellular functions. Twit Text FOAVip Skp2-Mediated RagA Ubiquitination Elicits a Negative Feedback to Prevent Amino-Acid-Dependent mTORC1 Hyperactivation by Recruiting GATOR1 ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=26051179 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26051179 #FOAvip English Wikipedia <ref>{{Cite pmid|26051179 }}</ref> Skp2-Mediated RagA Ubiquitination Elicits a Negative Feedback to Prevent Amino-Acid-Dependent mTORC1 Hyperactivation by Recruiting GATOR1 #MMPMID26051179 Jin G ; Lee SW ; Zhang X ; Cai Z ; Gao Y ; Chou PC ; Rezaeian AH ; Han F ; Wang CY ; Yao JC ; Gong Z ; Chan CH ; Huang CY ; Tsai FJ ; Tsai CH ; Tu SH ; Wu CH ; Sarbassov dos D ; Ho YS ; Lin HK Mol Cell 2015[Jun]; 58 (6 ): 989-1000 PMID26051179 show ga The regulation of RagA(GTP) is important for amino-acid-induced mTORC1 activation. Although GATOR1 complex has been identified as a negative regulator for mTORC1 by hydrolyzing RagA(GTP), how GATOR1 is recruited to RagA to attenuate mTORC1 signaling remains unclear. Moreover, how mTORC1 signaling is terminated upon amino acid stimulation is also unknown. We show that the recruitment of GATOR1 to RagA is induced by amino acids in an mTORC1-dependent manner. Skp2 E3 ligase drives K63-linked ubiquitination of RagA, which facilitates GATOR1 recruitment and RagA(GTP) hydrolysis, thereby providing a negative feedback loop to attenuate mTORC1 lysosomal recruitment and prevent mTORC1 hyperactivation. We further demonstrate that Skp2 promotes autophagy but inhibits cell size and cilia growth through RagA ubiquitination and mTORC1 inhibition. We thereby propose a negative feedback whereby Skp2-mediated RagA ubiquitination recruits GATOR1 to restrict mTORC1 signaling upon sustained amino acid stimulation, which serves a critical mechanism to maintain proper cellular functions. |Amino Acids/*pharmacology [MESH] |Animals [MESH] |Autophagy/genetics [MESH] |Cell Line, Tumor [MESH] |Enzyme Activation/drug effects [MESH] |Feedback, Physiological/drug effects [MESH] |Guanosine Triphosphate/metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Immunoblotting [MESH] |Lysine/metabolism [MESH] |Lysosomes/metabolism [MESH] |Mechanistic Target of Rapamycin Complex 1 [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Microscopy, Confocal [MESH] |Models, Biological [MESH] |Monomeric GTP-Binding Proteins/*metabolism [MESH] |Multiprotein Complexes/*metabolism [MESH] |NIH 3T3 Cells [MESH] |Protein Binding/drug effects [MESH] |RNA Interference [MESH] |S-Phase Kinase-Associated Proteins/genetics/*metabolism [MESH] |TOR Serine-Threonine Kinases/*metabolism [MESH]Skp2-Mediated RagA Ubiquitination Elicits a Negative Feedback to Preve(epmc).pdf DeepDyve Pubget Overpricing