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10.1074/jbc.274.11.7059 http://scihub22266oqcxt.onion/10.1074/jbc.274.11.7059 10066762!ä!10066762 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=10066762&cmd=llinks): Failed to open stream: HTTP request failed! 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Fas-induced B cell apoptosis requires an increase in free cytosolic magnesium as an early event |pdf=|usr=}}{{10066762}} gab.com Text Fas-induced B cell apoptosis requires an increase in free cytosolic magnesium as an early event JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=10066762 #FOAvip Ligation of the Fas molecule expressed on the surface of a cell initiates multiple signaling pathways that result in the apoptotic death of that cell. We have examined Mg2+ mobilization as well as Ca2+ mobilization in B cells undergoing Fas-initiated apoptosis. Our results indicate that cytosolic levels of free (non-complexed) Mg2+ ([Mg2+]i) and Ca2+ ([Ca2+]i) increase in cells undergoing apoptosis. Furthermore, the percentages of cells mobilizing Mg2+, fragmenting DNA, or externalizing phosphatidylserine (PS) increase in parallel as the concentration of anti-Fas monoclonal antibody is raised. Kinetic analysis suggests that Mg2+ mobilization is an early event in apoptosis, clearly preceding DNA fragmentation and probably occurring prior to externalization of PS as well. The source of Mg2+ that produces the increases in [Mg2+]i is intracellular and most likely is the mitochondria. Extended pretreatment of B cells with carbonyl cyanide m-chlorophenylhydrazone, an inhibitor of mitochondrial oxidative phosphorylation, produces proportional decreases in the percentage of cells mobilizing Mg2+, fragmenting DNA, and externalizing PS in response to anti-Fas monoclonal antibody treatment. These observations are consistent with the hypothesis that elevated [Mg2+]i is required for apoptosis. Furthermore, we propose that the increases in [Mg2+]i function not only as cofactors for Mg2+-dependent endonucleases, but also to facilitate the release of cytochrome c from the mitochondria, which drives many of the post-mitochondrial, caspase-mediated events in apoptotic cells. Twit Text FOAVip Fas-induced B cell apoptosis requires an increase in free cytosolic magnesium as an early event ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=10066762 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=10066762 #FOAvip English Wikipedia <ref>{{Cite pmid|10066762}}</ref> Fas-induced B cell apoptosis requires an increase in free cytosolic magnesium as an early event #MMPMID10066762 Chien MM; Zahradka KE; Newell MK; Freed JH J Biol Chem 1999[Mar]; 274 (11): 7059-66 PMID10066762show ga Ligation of the Fas molecule expressed on the surface of a cell initiates multiple signaling pathways that result in the apoptotic death of that cell. We have examined Mg2+ mobilization as well as Ca2+ mobilization in B cells undergoing Fas-initiated apoptosis. Our results indicate that cytosolic levels of free (non-complexed) Mg2+ ([Mg2+]i) and Ca2+ ([Ca2+]i) increase in cells undergoing apoptosis. Furthermore, the percentages of cells mobilizing Mg2+, fragmenting DNA, or externalizing phosphatidylserine (PS) increase in parallel as the concentration of anti-Fas monoclonal antibody is raised. Kinetic analysis suggests that Mg2+ mobilization is an early event in apoptosis, clearly preceding DNA fragmentation and probably occurring prior to externalization of PS as well. The source of Mg2+ that produces the increases in [Mg2+]i is intracellular and most likely is the mitochondria. Extended pretreatment of B cells with carbonyl cyanide m-chlorophenylhydrazone, an inhibitor of mitochondrial oxidative phosphorylation, produces proportional decreases in the percentage of cells mobilizing Mg2+, fragmenting DNA, and externalizing PS in response to anti-Fas monoclonal antibody treatment. These observations are consistent with the hypothesis that elevated [Mg2+]i is required for apoptosis. Furthermore, we propose that the increases in [Mg2+]i function not only as cofactors for Mg2+-dependent endonucleases, but also to facilitate the release of cytochrome c from the mitochondria, which drives many of the post-mitochondrial, caspase-mediated events in apoptotic cells. |Animals[MESH] |Antibodies, Monoclonal/immunology[MESH] |Apoptosis/*immunology[MESH] |B-Lymphocytes/*cytology/immunology[MESH] |CD40 Antigens/immunology[MESH] |Calcium/metabolism[MESH] |Cytosol/*metabolism[MESH] |Ionomycin/pharmacology[MESH] |Kinetics[MESH] |Lymphoma, B-Cell/metabolism/pathology[MESH] |Magnesium/*metabolism[MESH] |Mice[MESH] |Second Messenger Systems[MESH] |Tumor Cells, Cultured[MESH]Fas-induced B cell apoptosis requires an increase in free cytosolic ma(epmc).pdf DeepDyve Pubget Overpricing