کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2052274 | 1074225 | 2005 | 6 صفحه PDF | دانلود رایگان |
Tumor necrosis factor alpha (TNF-α) is one of the best-described cell death promoters. In murine L929 fibroblasts, dexamethasone inhibits TNF-α-induced cytotoxicity. Since phosphatidyl inositol 3 kinase (PI3K) and nuclear factor kappa B (NF-κB) proteins regulate several survival pathways, we evaluated their participation in dexamethasone protection against TNF-α cell death. We interfered with these pathways by overexpressing a negative dominant mutant of PI3K or a non-degradable mutant of inhibitor of NF-κB alpha (IκBα) (the cytoplasmic inhibitor of NF-κB) in L929 cells. The mutant IκB, but not the mutant PI3K, abrogated dexamethasone-mediated protection. The loss of dexamethasone protection was associated with a diminished accumulation in XIAP and c-IAP proteins.
Journal: FEBS Letters - Volume 579, Issue 18, 18 July 2005, Pages 3947–3952