کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1964272 | 1058538 | 2007 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Raf-1 and B-Raf promote protein kinase C θ interaction with BAD
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
PKCθ regulates the proliferation, survival and differentiation of T-cells. Here we show that PKCθ interacts with Raf-1 and B-Raf kinases. Raf-1 enhanced the kinase activity of associated PKCθ, while PKCθ reduced the catalytic activity of associated Raf-1. In contrast, B-Raf binding did not affect PKCθ kinase activity, and PKCθ did not change B-Raf activity. Coexpression of mutationally activated Raf-1 in cells enhanced the phosphorylation of T538 in the PKCθ activation loop. PKCθ and Raf cooperated in terms of binding to BAD, a pro-apoptotic Bcl-2 family protein that is inactivated by phosphorylation. While neither Raf-1 nor B-Raf could phosphorylate BAD, they enhanced the ability of PKCθ to interact with BAD and to phosphorylate BAD in vitro and in vivo, suggesting a new role for Raf proteins in T-cells by targeting PKCθ to interact with and phosphorylate BAD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 19, Issue 3, March 2007, Pages 547-555
Journal: Cellular Signalling - Volume 19, Issue 3, March 2007, Pages 547-555
نویسندگان
Alison Hindley, Walter Kolch,