期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 286, 期 45, 页码 39259-39268出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M111.255489
关键词
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资金
- Ministry of Education, Culture, Sports, Science, and Technology
- Grants-in-Aid for Scientific Research [23102010, 11J03194, 23102001] Funding Source: KAKEN
Immense previous efforts have elucidated the core machinery in cell migration, actin remodeling regulated by Rho family small GTPases including RhoA, Cdc42, and Rac1; however, the spatiotemporal regulation of these molecules remains largely unknown. Here, we report that EGF induces biphasic Rac1 activation in the process of cell migration, and UTKO1, a cell migration inhibitor, inhibits the second EGF-induced wave of Rac1 activation but not the first wave. To address the regulation mechanism and role of the second wave of Rac1 activation, we identified 14-3-3 xi as a target protein of UTKO1 and also showed that UTKO1 abrogated the binding of 14-3-3 xi to Tiam1 that was responsible for the second wave of Rac1 activation, suggesting that the interaction of 14-3-3 xi with Tiam1 is involved in this event. To our knowledge, this is the first report to use a chemical genetic approach to demonstrate the mechanism of temporal activation of Rac1.
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