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10.1038/ncb3064 http://scihub22266oqcxt.onion/10.1038/ncb3064 25402683!4894846!25402683     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Cell+Biol 2014 ; 16 (12): 1180-91 Nephropedia Template TP {{tp|p=25402683|t=2014. Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice |pdf=|usr=}}{{25402683}} gab.com Text Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice JO: Nat Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25402683 #FOAvip Ferroptosis is a non-apoptotic form of cell death induced by small molecules in specific tumour types, and in engineered cells overexpressing oncogenic RAS. Yet, its relevance in non-transformed cells and tissues is unexplored and remains enigmatic. Here, we provide direct genetic evidence that the knockout of glutathione peroxidase 4 (Gpx4) causes cell death in a pathologically relevant form of ferroptosis. Using inducible Gpx4(-/-) mice, we elucidate an essential role for the glutathione/Gpx4 axis in preventing lipid-oxidation-induced acute renal failure and associated death. We furthermore systematically evaluated a library of small molecules for possible ferroptosis inhibitors, leading to the discovery of a potent spiroquinoxalinamine derivative called Liproxstatin-1, which is able to suppress ferroptosis in cells, in Gpx4(-/-) mice, and in a pre-clinical model of ischaemia/reperfusion-induced hepatic damage. In sum, we demonstrate that ferroptosis is a pervasive and dynamic form of cell death, which, when impeded, promises substantial cytoprotection. Twit Text FOAVip Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice ????Nat Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25402683 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25402683 #FOAvip English Wikipedia <ref>{{Cite pmid|25402683}}</ref> Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice #MMPMID25402683 Friedmann Angeli JP; Schneider M; Proneth B; Tyurina YY; Tyurin VA; Hammond VJ; Herbach N; Aichler M; Walch A; Eggenhofer E; Basavarajappa D; Radmark O; Kobayashi S; Seibt T; Beck H; Neff F; Esposito I; Wanke R; Forster H; Yefremova O; Heinrichmeyer M; Bornkamm GW; Geissler EK; Thomas SB; Stockwell BR; O'Donnell VB; Kagan VE; Schick JA; Conrad M Nat Cell Biol 2014[Dec]; 16 (12): 1180-91 PMID25402683show ga Ferroptosis is a non-apoptotic form of cell death induced by small molecules in specific tumour types, and in engineered cells overexpressing oncogenic RAS. Yet, its relevance in non-transformed cells and tissues is unexplored and remains enigmatic. Here, we provide direct genetic evidence that the knockout of glutathione peroxidase 4 (Gpx4) causes cell death in a pathologically relevant form of ferroptosis. Using inducible Gpx4(-/-) mice, we elucidate an essential role for the glutathione/Gpx4 axis in preventing lipid-oxidation-induced acute renal failure and associated death. We furthermore systematically evaluated a library of small molecules for possible ferroptosis inhibitors, leading to the discovery of a potent spiroquinoxalinamine derivative called Liproxstatin-1, which is able to suppress ferroptosis in cells, in Gpx4(-/-) mice, and in a pre-clinical model of ischaemia/reperfusion-induced hepatic damage. In sum, we demonstrate that ferroptosis is a pervasive and dynamic form of cell death, which, when impeded, promises substantial cytoprotection. |*Apoptosis[MESH] |Acute Kidney Injury/*pathology[MESH] |Animals[MESH] |Arachidonate 12-Lipoxygenase/metabolism[MESH] |Arachidonate 15-Lipoxygenase/metabolism[MESH] |Cardiolipins/metabolism[MESH] |Cell Line[MESH] |Glutathione Peroxidase/*genetics[MESH] |Humans[MESH] |Imidazoles/pharmacology[MESH] |In Situ Nick-End Labeling[MESH] |Indoles/pharmacology[MESH] |Kidney/metabolism/pathology[MESH] |Lipid Peroxidation[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Mitochondria/metabolism[MESH] |Peroxidases/pharmacology[MESH] |Phosphatidylcholines/metabolism[MESH] |Phosphatidylethanolamines/metabolism[MESH] |Phospholipid Hydroperoxide Glutathione Peroxidase[MESH] |Quinoxalines/*pharmacology[MESH] |Reperfusion Injury/*pathology[MESH]Inactivation of the ferroptosis regulator Gpx4 triggers acute renal fa(epmc).pdf DeepDyve Pubget Overpricing