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FRS2 alpha is Essential for the Fibroblast Growth Factor to Regulate the mTOR Pathway and Autophagy in Mouse Embryonic Fibroblasts
Wallace L. ; Zhang, Yongyou ; Liu, Leyuan ; McKeehan ; Wang, Fen ( Texas A&M Hlth Sci Ctr) ; Lin, Xiang ; Shen, Yuemao ; Shen YM(沈月毛) ; Song, Siyang ; Song SY(宋思扬)
2011
关键词FGF autophagy mouse embryonic fibroblast receptor tyrosine kinase cell signaling
英文摘要Although the fibroblast growth factor (FGF) signaling axis plays important roles in cell survival, proliferation, and differentiation, the molecular mechanism underlying how the FGF elicits these diverse regulatory signals is not well understood. By using the Frs2 alpha null mouse embryonic fibroblast (MEF) in conjunction with inhibitors to multiple signaling pathways, here we report that the FGF signaling axis activates mTOR via the FGF receptor substrate 2 alpha (FRS2 alpha)-mediated PI3K/Akt pathway, and suppresses autophagy activity in MEFs. In addition, the PI3K/Akt pathway regulated mTOR is crucial for the FGF signaling axis to suppress autophagy in MEFs. Since autophagy has been proposed to play important roles in cell survival, proliferation, and differentiation, the findings suggest a novel mechanism for the FGF signaling axis to transmit regulatory signals to downstream effectors.; NCI[CA96824, P50 CA140388]; Cancer Prevention & Research Institute of Texas[RP110555]
语种英语
出版者IVYSPRING INT PUBL
内容类型期刊论文
源URL[http://dx.doi.org/doi:10.7150/ijbs.7.1114]  
专题生命科学-已发表论文
推荐引用方式
GB/T 7714
Wallace L.,Zhang, Yongyou,Liu, Leyuan,et al. FRS2 alpha is Essential for the Fibroblast Growth Factor to Regulate the mTOR Pathway and Autophagy in Mouse Embryonic Fibroblasts[J],2011.
APA Wallace L..,Zhang, Yongyou.,Liu, Leyuan.,McKeehan.,Wang, Fen .,...&宋思扬.(2011).FRS2 alpha is Essential for the Fibroblast Growth Factor to Regulate the mTOR Pathway and Autophagy in Mouse Embryonic Fibroblasts..
MLA Wallace L.,et al."FRS2 alpha is Essential for the Fibroblast Growth Factor to Regulate the mTOR Pathway and Autophagy in Mouse Embryonic Fibroblasts".(2011).
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