کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1936068 | 1050682 | 2007 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epidermal growth factor- and stress-induced loss of gap junctional communication is mediated by ERK-1/ERK-2 but not ERK-5 in rat liver epithelial cells
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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
Extracellular signal-regulated kinases (ERK) 1 and 2 as well as ERK-5 were previously suggested to phosphorylate connexin-43 and to contribute to the modulation of gap junctional intercellular communication (GJC). Exposure of rat liver epithelial cells to epidermal growth factor (EGF) or the redox cycling and alkylating agent menadione resulted in phosphorylation of connexin-43 and loss in GJC, both of which were abrogated by pharmacological inhibitors of ERK-1/2 activation, if used in concentrations that selectively abrogate phosphorylation of ERK-1/2 but not of ERK-5. Thus, EGF- or menadione-induced loss of GJC is mediated by ERK-1/2 but not ERK-5 in rat liver epithelial cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 364, Issue 2, 14 December 2007, Pages 313–317
Journal: Biochemical and Biophysical Research Communications - Volume 364, Issue 2, 14 December 2007, Pages 313–317
نویسندگان
Kotb Abdelmohsen, Elisabeth Sauerbier, Niloofar Ale-Agha, Juliane Beier, Philippe Walter, Stefanie Galban, Dominik Stuhlmann, Helmut Sies, Lars-Oliver Klotz,