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10.1128/MCB.00236-16 http://scihub22266oqcxt.onion/10.1128/MCB.00236-16 C5192080!5192080!27795296     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell+Biol 2017 ; 37 (1): ä Nephropedia Template TP {{tp|p=27795296|t=2017. PHD2 Is a Regulator for Glycolytic Reprogramming in Macrophages |pdf=|usr=}}{{27795296}} gab.com Text PHD2 Is a Regulator for Glycolytic Reprogramming in Macrophages JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27795296 #FOAvip The prolyl-4-hydroxylase domain (PHD) enzymes are regarded as the molecular oxygen sensors. There is an interplay between oxygen availability and cellular metabolism, which in turn has significant effects on the functionality of innate immune cells, such as macrophages. However, if and how PHD enzymes affect macrophage metabolism are enigmatic. We hypothesized that macrophage metabolism and function can be controlled via manipulation of PHD2. We characterized the metabolic phenotypes of PHD2-deficient RAW cells and primary PHD2 knockout bone marrow-derived macrophages (BMDM). Both showed typical features of anaerobic glycolysis, which were paralleled by increased pyruvate dehydrogenase kinase 1 (PDK1) protein levels and a decreased pyruvate dehydrogenase enzyme activity. Metabolic alterations were associated with an impaired cellular functionality. Inhibition of PDK1 or knockout of hypoxia-inducible factor 1? (HIF-1?) reversed the metabolic phenotype and impaired the functionality of the PHD2-deficient RAW cells and BMDM. Taking these results together, we identified a critical role of PHD2 for a reversible glycolytic reprogramming in macrophages with a direct impact on their function. We suggest that PHD2 serves as an adjustable switch to control macrophage behavior. Twit Text FOAVip PHD2 Is a Regulator for Glycolytic Reprogramming in Macrophages ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27795296 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27795296 #FOAvip English Wikipedia <ref>{{Cite pmid|27795296}}</ref> PHD2 Is a Regulator for Glycolytic Reprogramming in Macrophages #MMPMID27795296 Guentsch A; Beneke A; Swain L; Farhat K; Nagarajan S; Wielockx B; Raithatha K; Dudek J; Rehling P; Zieseniss A; Jatho A; Chong M; Santos CXC; Shah AM; Katschinski DM Mol Cell Biol 2017[Jan]; 37 (1): ä PMID27795296show ga The prolyl-4-hydroxylase domain (PHD) enzymes are regarded as the molecular oxygen sensors. There is an interplay between oxygen availability and cellular metabolism, which in turn has significant effects on the functionality of innate immune cells, such as macrophages. However, if and how PHD enzymes affect macrophage metabolism are enigmatic. We hypothesized that macrophage metabolism and function can be controlled via manipulation of PHD2. We characterized the metabolic phenotypes of PHD2-deficient RAW cells and primary PHD2 knockout bone marrow-derived macrophages (BMDM). Both showed typical features of anaerobic glycolysis, which were paralleled by increased pyruvate dehydrogenase kinase 1 (PDK1) protein levels and a decreased pyruvate dehydrogenase enzyme activity. Metabolic alterations were associated with an impaired cellular functionality. Inhibition of PDK1 or knockout of hypoxia-inducible factor 1? (HIF-1?) reversed the metabolic phenotype and impaired the functionality of the PHD2-deficient RAW cells and BMDM. Taking these results together, we identified a critical role of PHD2 for a reversible glycolytic reprogramming in macrophages with a direct impact on their function. We suggest that PHD2 serves as an adjustable switch to control macrophage behavior. äPHD2 Is a Regulator for Glycolytic Reprogramming in Macrophages (epmc).pdf DeepDyve Pubget Overpricing