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10.7554/eLife.22477 http://scihub22266oqcxt.onion/10.7554/eLife.22477 C5495572!5495572!28644127     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 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       eLife 2017 ; 6 (ä): ä Nephropedia Template TP {{tp|p=28644127|t=2017. MPI depletion enhances O-GlcNAcylation of p53 and suppresses the Warburg effect |pdf=|usr=}}{{28644127}} gab.com Text MPI depletion enhances O-GlcNAcylation of p53 and suppresses the Warburg effect JO: eLife http://www.kidney.de/pget.php?&tw=1&pmid=28644127 #FOAvip Rapid cellular proliferation in early development and cancer depends on glucose metabolism to fuel macromolecule biosynthesis. Metabolic enzymes are presumed regulators of this glycolysis-driven metabolic program, known as the Warburg effect; however, few have been identified. We uncover a previously unappreciated role for Mannose phosphate isomerase (MPI) as a metabolic enzyme required to maintain Warburg metabolism in zebrafish embryos and in both primary and malignant mammalian cells. The functional consequences of MPI loss are striking: glycolysis is blocked and cells die. These phenotypes are caused by induction of p53 and accumulation of the glycolytic intermediate fructose 6-phosphate, leading to engagement of the hexosamine biosynthetic pathway (HBP), increased O-GlcNAcylation, and p53 stabilization. Inhibiting the HBP through genetic and chemical methods reverses p53 stabilization and rescues the Mpi-deficient phenotype. This work provides mechanistic evidence by which MPI loss induces p53, and identifies MPI as a novel regulator of p53 and Warburg metabolism.DOI:http://dx.doi.org/10.7554/eLife.22477.001 Twit Text FOAVip MPI depletion enhances O-GlcNAcylation of p53 and suppresses the Warburg effect ????eLife http://www.kidney.de/pget.php?&tw=1&pmid=28644127 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28644127 #FOAvip English Wikipedia <ref>{{Cite pmid|28644127}}</ref> MPI depletion enhances O-GlcNAcylation of p53 and suppresses the Warburg effect #MMPMID28644127 Shtraizent N; DeRossi C; Nayar S; Sachidanandam R; Katz LS; Prince A; Koh AP; Vincek A; Hadas Y; Hoshida Y; Scott DK; Eliyahu E; Freeze HH; Sadler KC; Chu J eLife 2017[]; 6 (ä): ä PMID28644127show ga Rapid cellular proliferation in early development and cancer depends on glucose metabolism to fuel macromolecule biosynthesis. Metabolic enzymes are presumed regulators of this glycolysis-driven metabolic program, known as the Warburg effect; however, few have been identified. We uncover a previously unappreciated role for Mannose phosphate isomerase (MPI) as a metabolic enzyme required to maintain Warburg metabolism in zebrafish embryos and in both primary and malignant mammalian cells. The functional consequences of MPI loss are striking: glycolysis is blocked and cells die. These phenotypes are caused by induction of p53 and accumulation of the glycolytic intermediate fructose 6-phosphate, leading to engagement of the hexosamine biosynthetic pathway (HBP), increased O-GlcNAcylation, and p53 stabilization. Inhibiting the HBP through genetic and chemical methods reverses p53 stabilization and rescues the Mpi-deficient phenotype. This work provides mechanistic evidence by which MPI loss induces p53, and identifies MPI as a novel regulator of p53 and Warburg metabolism.DOI:http://dx.doi.org/10.7554/eLife.22477.001 äMPI depletion enhances O-GlcNAcylation of p53 and suppresses the Warbu(epmc).pdf DeepDyve Pubget Overpricing