原创力文档tbc1d3, a hominoid-specific gene, delays irs-1 degradation and promotes insulin signaling by modulating p70 s6 kinase activitytbc1d3 hominoid-specific基因,延迟irs-1退化和促进胰岛素信号由调制p70 s6激酶活性.pdfVIP
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tbc1d3, a hominoid-specific gene, delays irs-1 degradation and promotes insulin signaling by modulating p70 s6 kinase activitytbc1d3 hominoid-specific基因,延迟irs-1退化和促进胰岛素信号由调制p70 s6激酶活性
TBC1D3, a Hominoid-Specific Gene, Delays IRS-1
Degradation and Promotes Insulin Signaling by
Modulating p70 S6 Kinase Activity
1.¤ 1. 1 1 1 1,2
Marisa J. Wainszelbaum , Jialu Liu , Chen Kong , Priya Srikanth , Dmitri Samovski , Xiong Su *,
Philip D. Stahl1*
1 Department of Cell Biology and Physiology, Center for Human Nutrition, Washington University School of Medicine, St. Louis, Missouri, United States of America,
2 Department of Internal Medicine, Center for Human Nutrition, Washington University School of Medicine, St. Louis, Missouri, United States of America
Abstract
Insulin/IGF-1 signaling plays a pivotal role in the regulation of cellular homeostasis through its control of glucose
metabolism as well as due to its effects on cell proliferation. Aberrant regulation of insulin signaling has been repeatedly
implicated in uncontrolled cell growth and malignant transformations. TBC1D3 is a hominoid specific gene previously
identified as an oncogene in breast and prostate cancers. Our efforts to identify the molecular mechanisms of TBC1D3-
induced oncogenesis revealed the role of TBC1D3 in insulin/IGF-1 signaling pathway. We document here that TBC1D3
intensifies insulin/IGF-1-induced signal transduction through intricate, yet elegant fine-tuning of signaling mechanisms. We
show that TBC1D3 expression substantially delayed ubiquitination and degradation of insulin receptor substrate-1 (IRS-1).
This effect is achieved through suppression of serine phosphorylation at S636/639, S307 and S312 of IRS-1, which are key
phosphorylation sites required for IRS-1 degradation. Furthermore, we report that the effect of
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