期刊
JOURNAL OF CELL BIOLOGY
卷 178, 期 2, 页码 245-255出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200604114
关键词
-
类别
资金
- Intramural NIH HHS Funding Source: Medline
At the plasma membrane, heterotrimeric G proteins act as molecular switches to relay signals from G protein-coupled receptors; however, G(alpha) subunits also have receptor-independent functions at intracellular sites. Regulator of G protein signaling (RGS) 14, which enhances the intrinsic GTPase activity of G(i alpha) proteins, localizes in centrosomes, which suggests the coexpression of G(i alpha). We show expression of G(i alpha 1), G(i alpha 2), and G(i alpha 3) in the centrosomes and at the midbody. Fluorescence resonance energy transfer analysis confirms a direct interaction between RGS14 and G(i alpha 1) in centrosomes. Expression of GTPase-deficient G(i alpha 1) results in defective cytokinesis, whereas that of wild-type or GTPase-deficient G(i alpha 3) causes prolonged mitosis. Cells treated with pertussis toxin, with reduced expression of G(i alpha 1), G(i alpha 2), and G(i alpha 3) or with decreased expression of RGS14 also exhibit cytokinesis defects. These results suggest that G(i alpha) proteins and their regulators at these sites may play essential roles during mammalian cell division.
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