کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738381 | 1046704 | 2011 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis
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کلمات کلیدی
FASNACDISCFADDGPx2N-acetylcysteine - N-استیل سیستئینApoptosis - خزان یاختهایFree radicals - رادیکال آزادHyperoxia - هیپوکسیاFAS-associated death domain protein - پروتئین دامنه مرگ مرتبط با FASdeath-inducing signaling complex - پیچیدگی سیگنالینگ ناشی از مرگcaveolin-1 - کائولین-1Catalase - کاتالازCav-1 - کاو-1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Fas-mediated apoptosis is a crucial cellular event. Fas, the Fas-associated death domain, and caspase 8 form the death-inducing signaling complex (DISC). Activated caspase 8 mediates the extrinsic pathways and cleaves cytosolic BID. Truncated BID (tBID) translocates to the mitochondria, facilitates the release of cytochrome c, and activates the intrinsic pathways. However, the mechanism causing these DISC components to aggregate and form the complex remains unclear. We found that Cav-1 regulated Fas signaling and mediated the communication between extrinsic and intrinsic pathways. Shortly after hyperoxia (4Â h), the colocalization and interaction of Cav-1 and Fas increased, followed by Fas multimer and DISC formation. Deletion of Cav-1 (Cav-1â/â) disrupted DISC formation. Further, Cav-1 interacted with BID. Mutation of Cav-1 Y14 tyrosine to phenylalanine (Y14F) disrupted the hyperoxia-induced interaction between BID and Cav-1 and subsequently yielded a decreased level of tBID and resistance to hyperoxia-induced apoptosis. The reactive oxygen species (ROS) scavenger N-acetylcysteine decreased the Cav-1-Fas interaction. Deletion of glutathione peroxidase-2 using siRNA aggravated the BID-Cav-1 interaction and tBID formation. Taken together, these results indicate that Cav-1 regulates hyperoxia/ROS-induced apoptosis through interactions with Fas and BID, probably via Fas palmitoylation and Cav-1 Y14 phosphorylation, respectively.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 50, Issue 10, 15 May 2011, Pages 1252-1262
Journal: Free Radical Biology and Medicine - Volume 50, Issue 10, 15 May 2011, Pages 1252-1262
نویسندگان
Meng Zhang, Seon-Jin Lee, ChangHyeok An, Jin-fu Xu, Bharat Joshi, Ivan R. Nabi, Augustine M.K. Choi, Yang Jin,