The TC10-interacting protein CIP4/2 is required for insulin-stimulated Glut4 translocation in 3T3L1 adipocytes
The TC10-interacting protein CIP4/2 is required for insulin-stimulated Glut4 translocation in 3T3L1 adipocytes
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DOI：
10.1073/pnas.202495599
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发表时间：
2002-10-01
影响因子：
11.1
通讯作者：
Saltiel, AR
中科院分区：
文献类型：
--
作者：
Chang, L;Adams, RD;Saltiel, AR
GTCRTC 10在胰岛素刺激的葡萄糖转运中起关键作用。我们在这里报告的识别TC 10相互作用蛋白CIP 4/2（Cdc 4/2相互作用蛋白4/2）作为在这一途径中的效应。CIP 4/2在基础条件下定位于细胞内区室，并在胰岛素刺激下易位至质膜。组成型活性TC 10的过表达将CIP 4/2带到质膜，而TC 10的抑制形式的过表达阻断胰岛素产生的CIP 4/2的易位。CIP 4/2的突变体形式含有N-末端缺失或减少TC 10结合的过表达抑制胰岛素刺激的Glut 4易位。这些数据表明，CIP 4/2可能发挥重要作用，在胰岛素刺激的葡萄糖转运作为下游效应的TC 10。
The GTPase TC10 plays a critical role in insulin-stimulated glucose transport. We report here the identification of the TC10-interacting protein CIP4/2 (Cdc42-interacting protein 4/2) as an effector in this pathway. CIP4/2 localizes to an intracellular compartment under basal conditions and translocates to the plasma membrane on insulin stimulation. Overexpression of constitutively active TC10 brings CIP4/2 to the plasma membrane, whereas overexpression of an inhibitory form of TC10 blocks the translocation of CIP4/2 produced by insulin. Overexpression of mutant forms of CIP4/2 containing an N-terminal deletion or with diminished TC10 binding inhibits insulin-stimulated Glut4 translocation. These data suggest that CIP4/2 may play an important role in insulin-stimulated glucose transport as a downstream effector of TC10.