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10.1016/j.cmet.2015.06.009 http://scihub22266oqcxt.onion/10.1016/j.cmet.2015.06.009 C4663076!4663076!26190651     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Metab 2015 ; 22 (3): 508-15 Nephropedia Template TP {{tp|p=26190651|t=2015. 2-Hydroxyglutarate Inhibits ATP Synthase and mTOR Signaling |pdf=|usr=}}{{26190651}} gab.com Text 2-Hydroxyglutarate Inhibits ATP Synthase and mTOR Signaling JO: Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=26190651 #FOAvip Recently we discovered that the central metabolite ?-ketoglutarate (?-KG) extends lifespan in C. elegans through inhibition of ATP synthase and TOR signaling. Unexpectedly, here we find that (R)-2-hydroxyglutarate ((R)-2HG), an oncometabolite that interferes with various ?-KG mediated processes, extends worm lifespan similarly. (R)-2HG accumulates in human cancers carrying neomorphic mutations in the isocitrate dehydrogenase (IDH) 1 and 2 genes. We show that, like ?-KG, both (R)-2HG and (S)-2HG bind and inhibit ATP synthase, and inhibit mTOR signaling; these effects are mirrored in IDH1 mutant cells, suggesting a growth suppressive function of (R)-2HG. Consistently, inhibition of ATP synthase by 2-HG or ?-KG in glioblastoma cells is sufficient for growth arrest and tumor cell killing under conditions of glucose limitation, such as when ketone bodies (instead of glucose) are supplied for energy. These findings inform therapeutic strategies and open avenues for investigating the roles of 2-HG and metabolites in biology and disease. Twit Text FOAVip 2-Hydroxyglutarate Inhibits ATP Synthase and mTOR Signaling ????Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=26190651 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26190651 #FOAvip English Wikipedia <ref>{{Cite pmid|26190651}}</ref> 2-Hydroxyglutarate Inhibits ATP Synthase and mTOR Signaling #MMPMID26190651 Fu X; Chin RM; Vergnes L; Hwang H; Deng G; Xing Y; Pai MY; Li S; Ta L; Fazlollahi F; Chen C; Prins RM; Teitell MA; Nathanson DA; Lai A; Faull KF; Jiang M; Clarke SG; Cloughesy TF; Graeber TG; Braas D; Christofk HR; Jung ME; Reue K; Huang J Cell Metab 2015[Sep]; 22 (3): 508-15 PMID26190651show ga Recently we discovered that the central metabolite ?-ketoglutarate (?-KG) extends lifespan in C. elegans through inhibition of ATP synthase and TOR signaling. Unexpectedly, here we find that (R)-2-hydroxyglutarate ((R)-2HG), an oncometabolite that interferes with various ?-KG mediated processes, extends worm lifespan similarly. (R)-2HG accumulates in human cancers carrying neomorphic mutations in the isocitrate dehydrogenase (IDH) 1 and 2 genes. We show that, like ?-KG, both (R)-2HG and (S)-2HG bind and inhibit ATP synthase, and inhibit mTOR signaling; these effects are mirrored in IDH1 mutant cells, suggesting a growth suppressive function of (R)-2HG. Consistently, inhibition of ATP synthase by 2-HG or ?-KG in glioblastoma cells is sufficient for growth arrest and tumor cell killing under conditions of glucose limitation, such as when ketone bodies (instead of glucose) are supplied for energy. These findings inform therapeutic strategies and open avenues for investigating the roles of 2-HG and metabolites in biology and disease. ä2-Hydroxyglutarate Inhibits ATP Synthase and mTOR Signaling (epmc).pdf DeepDyve Pubget Overpricing