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10.1007/s00018-016-2194-1 http://scihub22266oqcxt.onion/10.1007/s00018-016-2194-1 C4887533!4887533 !27048822     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27048822 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27048822 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Mol+Life+Sci 2016 ; 73 (11-12 ): 2195-209 Nephropedia Template TP {{tp|p=27048822 |t=2016. Mechanisms of ferroptosis |pdf=|usr=}}{{27048822 }} gab.com Text Mechanisms of ferroptosis JO: Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=27048822 #FOAvip Ferroptosis is a non-apoptotic form of cell death that can be triggered by small molecules or conditions that inhibit glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4). This lethal process is defined by the iron-dependent accumulation of lipid reactive oxygen species and depletion of plasma membrane polyunsaturated fatty acids. Cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression may be sensitized to this process. Conversely, a number of small molecule inhibitors of ferroptosis have been identified, including ferrostatin-1 and liproxstatin-1, which can block pathological cell death events in brain, kidney and other tissues. Recent work has identified a number of genes required for ferroptosis, including those involved in lipid and amino acid metabolism. Outstanding questions include the relationship between ferroptosis and other forms of cell death, and whether activation or inhibition of ferroptosis can be exploited to achieve desirable therapeutic ends. Twit Text FOAVip Mechanisms of ferroptosis ????Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=27048822 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27048822 #FOAvip English Wikipedia <ref>{{Cite pmid|27048822 }}</ref> Mechanisms of ferroptosis #MMPMID27048822 Cao JY ; Dixon SJ Cell Mol Life Sci 2016[Jun]; 73 (11-12 ): 2195-209 PMID27048822 show ga Ferroptosis is a non-apoptotic form of cell death that can be triggered by small molecules or conditions that inhibit glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4). This lethal process is defined by the iron-dependent accumulation of lipid reactive oxygen species and depletion of plasma membrane polyunsaturated fatty acids. Cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression may be sensitized to this process. Conversely, a number of small molecule inhibitors of ferroptosis have been identified, including ferrostatin-1 and liproxstatin-1, which can block pathological cell death events in brain, kidney and other tissues. Recent work has identified a number of genes required for ferroptosis, including those involved in lipid and amino acid metabolism. Outstanding questions include the relationship between ferroptosis and other forms of cell death, and whether activation or inhibition of ferroptosis can be exploited to achieve desirable therapeutic ends. |Cell Death/*physiology [MESH] |Cell Membrane/*pathology [MESH] |Cyclohexylamines/pharmacology [MESH] |Fatty Acids, Unsaturated/metabolism [MESH] |Glutathione Peroxidase/biosynthesis/*metabolism [MESH] |Glutathione/biosynthesis/*metabolism [MESH] |Iron/metabolism [MESH] |Neoplasms/*pathology [MESH] |Phenylenediamines/pharmacology [MESH] |Phospholipid Hydroperoxide Glutathione Peroxidase [MESH] |Quinoxalines/pharmacology [MESH] |Reactive Oxygen Species/*metabolism [MESH]Mechanisms of ferroptosis (epmc).pdf DeepDyve Pubget Overpricing