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10.1016/j.cell.2013.12.010 http://scihub22266oqcxt.onion/10.1016/j.cell.2013.12.010 24439385!4076414!24439385     free     free     free       Cell 2014 ; 156 (1-2): 317-331 Nephropedia Template TP {{tp|p=24439385|t=2014. Regulation of ferroptotic cancer cell death by GPX4 |pdf=|usr=}}{{24439385}} gab.com Text Regulation of ferroptotic cancer cell death by GPX4 JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=24439385 #FOAvip Ferroptosis is a form of nonapoptotic cell death for which key regulators remain unknown. We sought a common mediator for the lethality of 12 ferroptosis-inducing small molecules. We used targeted metabolomic profiling to discover that depletion of glutathione causes inactivation of glutathione peroxidases (GPXs) in response to one class of compounds and a chemoproteomics strategy to discover that GPX4 is directly inhibited by a second class of compounds. GPX4 overexpression and knockdown modulated the lethality of 12 ferroptosis inducers, but not of 11 compounds with other lethal mechanisms. In addition, two representative ferroptosis inducers prevented tumor growth in xenograft mouse tumor models. Sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPX4-regulated ferroptosis. Thus, GPX4 is an essential regulator of ferroptotic cancer cell death. Twit Text FOAVip Regulation of ferroptotic cancer cell death by GPX4 ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=24439385 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24439385 #FOAvip English Wikipedia <ref>{{Cite pmid|24439385}}</ref> Regulation of ferroptotic cancer cell death by GPX4 #MMPMID24439385 Yang WS; SriRamaratnam R; Welsch ME; Shimada K; Skouta R; Viswanathan VS; Cheah JH; Clemons PA; Shamji AF; Clish CB; Brown LM; Girotti AW; Cornish VW; Schreiber SL; Stockwell BR Cell 2014[Jan]; 156 (1-2): 317-331 PMID24439385show ga Ferroptosis is a form of nonapoptotic cell death for which key regulators remain unknown. We sought a common mediator for the lethality of 12 ferroptosis-inducing small molecules. We used targeted metabolomic profiling to discover that depletion of glutathione causes inactivation of glutathione peroxidases (GPXs) in response to one class of compounds and a chemoproteomics strategy to discover that GPX4 is directly inhibited by a second class of compounds. GPX4 overexpression and knockdown modulated the lethality of 12 ferroptosis inducers, but not of 11 compounds with other lethal mechanisms. In addition, two representative ferroptosis inducers prevented tumor growth in xenograft mouse tumor models. Sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPX4-regulated ferroptosis. Thus, GPX4 is an essential regulator of ferroptotic cancer cell death. |Animals[MESH] |Carbolines/*pharmacology[MESH] |Carcinoma, Renal Cell/drug therapy[MESH] |Cell Death/*drug effects[MESH] |Cell Line, Tumor[MESH] |Gene Knockdown Techniques[MESH] |Glutathione Peroxidase/*antagonists & inhibitors/genetics/metabolism[MESH] |Glutathione/metabolism[MESH] |Heterografts[MESH] |Humans[MESH] |Lymphoma, B-Cell/drug therapy[MESH] |Mice[MESH] |Neoplasm Transplantation[MESH] |Neoplasms/drug therapy[MESH] |Phospholipid Hydroperoxide Glutathione Peroxidase[MESH]Regulation of ferroptotic cancer cell death by GPX4 (epmc).pdf DeepDyve Pubget Overpricing