Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26190651 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       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 We discovered recently that the central metabolite ?-ketoglutarate (?-KG) extends the lifespan of C. elegans through inhibition of ATP synthase and TOR signaling. Here we find, unexpectedly, that (R)-2-hydroxyglutarate ((R)-2HG), an oncometabolite that interferes with various ?-KG-mediated processes, similarly extends worm lifespan. (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, e.g., 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 PMID26190651 show ga We discovered recently that the central metabolite ?-ketoglutarate (?-KG) extends the lifespan of C. elegans through inhibition of ATP synthase and TOR signaling. Here we find, unexpectedly, that (R)-2-hydroxyglutarate ((R)-2HG), an oncometabolite that interferes with various ?-KG-mediated processes, similarly extends worm lifespan. (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, e.g., 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. |*Signal Transduction [MESH] |Adenosine Triphosphatases/*metabolism [MESH] |Animals [MESH] |Caenorhabditis elegans/*physiology [MESH] |Cell Proliferation [MESH] |Glioblastoma/genetics/*metabolism [MESH] |Glutarates/*metabolism [MESH] |Humans [MESH] |Isocitrate Dehydrogenase/genetics/metabolism [MESH] |Longevity [MESH] |Mutation [MESH]2-Hydroxyglutarate Inhibits ATP Synthase and mTOR Signaling (epmc).pdf DeepDyve Pubget Overpricing