کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815851 | 1058506 | 2010 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Endothelin-1 induces p66Shc activation through EGF receptor transactivation: Role of β1Pix/Gαi3 interaction
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Endothelin-1 (ET-1) is a vasoconstrictor peptide known to be a potent mitogen for glomerular mesangial cells. We have shown that ET-1 stimulates the adaptor protein p66Shc through Rac/Cdc42 guanine nucleotide exchange factor β1Pix. In this study, we demonstrate that ET-1-induced serine phosphorylation of p66Shc is mediated through Gαi3. Pertussis toxin treatment of cells induced a significant decrease in the interaction between β1Pix and ETA-R, and an increase in the binding of Gαi3 and Gβ1 to β1Pix. Activation of heterotrimeric G proteins by AlF4â resulted in an increase of Gαi3 binding to β1Pix, which was significantly disrupted in cells expressing β1Pix dimerization deficient mutant, β1PixÎ (602-611). In cells expressing β1PixÎ (602-611), ET-1-induced p66Shc activation was also significantly decreased. Specific inhibition of EGF receptor by AG1478 blocked ET-1-induced p66Shc activation and the binding of p66Shc and Gαi3 to β1Pix. Inhibition of Erk1/2 blocked p66Shc activation induced by ET-1. Altogether, our results indicate that ET-1 activates p66Shc through EGF receptor transactivation, leading to the activation of Gαi3, β1Pix and Erk1/2.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 22, Issue 2, February 2010, Pages 325-329
Journal: Cellular Signalling - Volume 22, Issue 2, February 2010, Pages 325-329
نویسندگان
Ahmed Chahdi, Andrey Sorokin,