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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
Rong, Zhili ; Ren, Yongming ; Cheng, Long ; Li, Zhiyong ; Li, Yinghua ; Sun, Yang ; Li, Hongge ; Xiong, Shiqin ; Chang, Zhijle
2010-05-11 ; 2010-05-11
关键词Sef-s Sef alternative splice FGF signaling ERK proliferation NON-AUG CODONS RECEPTOR TYROSINE KINASES TRANSLATIONAL INITIATION CUG EXPRESSION FEEDBACK SPROUTY PHOSPHORYLATION EMBRYOGENESIS PATTERN Cell Biology
中文摘要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 Sell 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. (c) 2006 Elsevier Inc. All rights reserved.
语种英语 ; 英语
出版者ELSEVIER SCIENCE INC ; NEW YORK ; 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
内容类型期刊论文
源URL[http://hdl.handle.net/123456789/26704]  
专题清华大学
推荐引用方式
GB/T 7714
Rong, Zhili,Ren, Yongming,Cheng, Long,et al. 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[J],2010, 2010.
APA Rong, Zhili.,Ren, Yongming.,Cheng, Long.,Li, Zhiyong.,Li, Yinghua.,...&Chang, Zhijle.(2010).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..
MLA Rong, Zhili,et al."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".(2010).
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