کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1964349 1058544 2007 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Sef-S, an alternative splice isoform of sef gene, inhibits NIH3T3 cell proliferation via a mitogen-activated protein kinases p42 and p44 (ERK1/2)-independent mechanism
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Sef-S, an alternative splice isoform of sef gene, inhibits NIH3T3 cell proliferation via a mitogen-activated protein kinases p42 and p44 (ERK1/2)-independent mechanism
چکیده انگلیسی

sef (similar expression to fgf genes) was recently identified as a negative regulator of fibroblast growth factor (FGF) signaling in zebrafish, chicken, mouse and human. By repressing events upstream and/or downstream Ras, Sef inhibits FGF-induced ERK activation and cell proliferation. Here we report that Sef-S, an alternative splice isoform of Sef, lacks a signal peptide and is localized in cytosol. Sef-S inhibits FGF-induced NIH3T3 cell proliferation, a similar function to Sef. However, Sef-S represses neither the intensity nor the duration of ERK activation. Moreover, Sef-S does not inhibit Elk1-dependent transcription. Our study revealed that the signal peptide is critical for the different activities between Sef and Sef-S in FGF-Ras-MAPK signaling cascades. Furthermore, we observed that Sef-S associated with FGFR2 in a co-immunoprecipitated complex. These results indicate that Sef-S inhibits FGF-induced NIH3T3 cell proliferation via an ERK-independent mechanism and therefore suggest that alternative splice licenses sef gene to inhibit cell proliferation via multiple signaling pathways.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 19, Issue 1, January 2007, Pages 93–102
نویسندگان
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