کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10905408 | 1086753 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The Fas-associated death domain protein/caspase-8/c-FLIP signaling pathway is involved in TNF-induced activation of ERK
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کلمات کلیدی
TNFRTNF receptor-associated death domain proteinzVAD.fmkMurine fibroblastsTRADDTRAFc-FLIPDEDFADDMBPbenzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone - بنزیلوکسیکربنیل-وال-آلا-آسپ-فلورومتیلیکونProliferation - ترویجdeath effector domain - دامنه موثر مرگTNF receptor-associated factor - عامل گیرنده TNFtumor necrosis factor - فاکتور نکروز تومورRIP - پاره کردنFAS-associated death domain protein - پروتئین دامنه مرگ مرتبط با FASMyelin basic protein - پروتئین پایه میلینFAN - پنکهextracellular signal-regulated kinases - کیناز های تنظیم شده سیگنال خارج سلولیTNF receptor - گیرنده TNF
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: The Fas-associated death domain protein/caspase-8/c-FLIP signaling pathway is involved in TNF-induced activation of ERK The Fas-associated death domain protein/caspase-8/c-FLIP signaling pathway is involved in TNF-induced activation of ERK](/preview/png/10905408.png)
چکیده انگلیسی
The cytokine TNF activates multiple signaling pathways leading to cellular responses ranging from proliferation and survival to apoptosis. While most of these pathways have been elucidated in detail over the past few years, the molecular mechanism leading to the activation of the MAP kinases ERK remains ill defined and is controversially discussed. Therefore, we have analyzed TNF-induced ERK activation in various human and murine cell lines and show that it occurs in a cell-type-specific manner. In addition, we provide evidence for the involvement of the signaling components Fas-associated death domain protein (FADD), caspase-8, and c-FLIP in the pathway activating ERK in response to TNF. This conclusion is based on the following observations: (I) Overexpression of FADD, caspase-8, or a c-FLIP protein containing the death effector domains only leads to enhanced and prolonged ERK activation after TNF treatment. (II) TNF-induced ERK activation is strongly diminished in the absence of FADD. Interestingly, the enzymatic function of caspase-8 is not required for TNF-induced ERK activation. Additional evidence suggests a role for this pathway in the proliferative response of murine fibroblasts to TNF.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 310, Issue 1, 15 October 2005, Pages 33-42
Journal: Experimental Cell Research - Volume 310, Issue 1, 15 October 2005, Pages 33-42
نویسندگان
Silke Lüschen, Markus Falk, Gudrun Scherer, Sandra Ussat, Maren Paulsen, Sabine Adam-Klages,