期刊
FEBS LETTERS
卷 588, 期 1, 页码 15-20出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2013.10.050
关键词
Beta-cell; TBC1D1; Proliferation; Apoptosis; Glucose response
资金
- Juvenile Diabetes Research Foundation (JDRF award) [31-2008-413]
- Swiss National Science Foundation [31003A_135645/1, 31003A_144092/1]
- Grants-in-Aid for Scientific Research [25293074] Funding Source: KAKEN
- Swiss National Science Foundation (SNF) [31003A_144092, 31003A_135645] Funding Source: Swiss National Science Foundation (SNF)
The Rab-GTPase activating protein TBC1D1 is a paralog of AS160/TBC1D4. AS160/TBC1D4, a downstream effector of Akt, has been shown to play a central role in beta-cell function and survival. The two proteins have overlapping function in insulin signalling in muscle cells. However, the expression and the potential role of TBC1D1 in beta-cells remain unknown. Therefore, the aim of this study is to investigate whether TBC1D1 is expressed in beta-cells and whether it plays, as AS160/TBC1D4, a role in beta-cell function and survival. Using human and rat beta-cells, this study shows for the first time that TBC1D1 is expressed and phosphorylated in response to glucose in these cells. Knockdown of TBC1D1 in beta-cells resulted in increased basal and glucose-stimulated insulin release, decreased proliferation but no change in apoptosis. Structured summary of protein interactions: TBC1D1, glucagon and insulin colocalize by fluorescence microscopy (View interaction) (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据