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10.1016/j.molcel.2017.01.027 http://scihub22266oqcxt.onion/10.1016/j.molcel.2017.01.027 C5389741!5389741!28238651     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 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\28238651.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Cell 2017 ; 65 (5): 917-931.e6 Nephropedia Template TP {{tp|p=28238651|t=2017. Phosphoglycerate kinase 1 phosphorylates Beclin1 to induce autophagy |pdf=|usr=}}{{28238651}} gab.com Text Phosphoglycerate kinase 1 phosphorylates Beclin1 to induce autophagy JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=28238651 #FOAvip Autophagy is crucial for maintaining cell homeostasis. However, the precise mechanism underlying autophagy initiation remains to be defined. Here, we demonstrate that glutamine deprivation and hypoxia result in inhibition of mTOR-mediated acetyl-transferase ARD1 S228 phosphorylation, leading to ARD1-dependent phosphoglycerate kinase 1 (PGK1) K388 acetylation and subsequent PGK1-mediated Beclin1 S30 phosphorylation. This phosphorylation enhances ATG14L-associated class III phosphatidylinositol 3-kinase VPS34 activity by increasing the binding of phosphatidylinositol to VPS34. ARD1-dependent PGK1 acetylation and PGK1-mediated Beclin1 S30 phosphorylation are required for glutamine deprivation- and hypoxia-induced autophagy and brain tumorigenesis. Furthermore, PGK1 K388 acetylation levels correlate with Beclin1 S30 phosphorylation levels and poor prognosis in glioblastoma patients. Our study unearthed an important mechanism underlying cellular stress-induced autophagy initiation, in which the protein kinase activity of the metabolic enzyme PGK1 plays an instrumental role, and revealed the significance of the mutual regulation of autophagy and cell metabolism in maintaining cell homeostasis. Twit Text FOAVip Phosphoglycerate kinase 1 phosphorylates Beclin1 to induce autophagy ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=28238651 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28238651 #FOAvip English Wikipedia <ref>{{Cite pmid|28238651}}</ref> Phosphoglycerate kinase 1 phosphorylates Beclin1 to induce autophagy #MMPMID28238651 Qian X; Li X; Cai Q; Zhang C; Jiang Y; Lee JH; Hawke D; Wang Y; Xia Y; Zheng Y; Jiang BH; Liu DX; Jiang T; Lu Z Mol Cell 2017[Mar]; 65 (5): 917-931.e6 PMID28238651show ga Autophagy is crucial for maintaining cell homeostasis. However, the precise mechanism underlying autophagy initiation remains to be defined. Here, we demonstrate that glutamine deprivation and hypoxia result in inhibition of mTOR-mediated acetyl-transferase ARD1 S228 phosphorylation, leading to ARD1-dependent phosphoglycerate kinase 1 (PGK1) K388 acetylation and subsequent PGK1-mediated Beclin1 S30 phosphorylation. This phosphorylation enhances ATG14L-associated class III phosphatidylinositol 3-kinase VPS34 activity by increasing the binding of phosphatidylinositol to VPS34. ARD1-dependent PGK1 acetylation and PGK1-mediated Beclin1 S30 phosphorylation are required for glutamine deprivation- and hypoxia-induced autophagy and brain tumorigenesis. Furthermore, PGK1 K388 acetylation levels correlate with Beclin1 S30 phosphorylation levels and poor prognosis in glioblastoma patients. Our study unearthed an important mechanism underlying cellular stress-induced autophagy initiation, in which the protein kinase activity of the metabolic enzyme PGK1 plays an instrumental role, and revealed the significance of the mutual regulation of autophagy and cell metabolism in maintaining cell homeostasis. äPhosphoglycerate kinase 1 phosphorylates Beclin1 to induce autophagy (epmc).pdf DeepDyve Pubget Overpricing