非典型激酶Cdk5被胰岛素激活，调节GLUT4与E-Syt1之间的关联，并调节3T3-L1脂肪细胞中的葡萄糖转运。
The atypical kinase Cdk5 is activated by insulin, regulates the association between GLUT4 and E-Syt1, and modulates glucose transport in 3T3-L1 adipocytes.
作者信息
Lalioti Vasiliki, Muruais Gemma, Dinarina Ana, van Damme Josef, Vandekerckhove Joel, Sandoval Ignacio V
机构信息
Department of Cell Biology and Immunology, Centro de Biologia Molecular Severo Ochoa, Universidad Autónoma de Madrid, 28049 Madrid, Spain.
出版信息
Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4249-53. doi: 10.1073/pnas.0900218106. Epub 2009 Mar 2.
Abstract
Here, we report that Cdk5 activation is stimulated by insulin and plays a key role in the regulation of GLUT4-mediated glucose uptake in 3T3-L1 adipocytes. Insulin activation of Cdk5 requires PI3K signaling. Insulin-activated Cdk5 phosphorylates E-Syt1, a 5 C2-domain protein-related to the synaptotagmins that is induced during adipocyte differentiation. Phosphorylated E-Syt1 associates with GLUT4, an event inhibited by the Cdks inhibitor roscovitine. Cdk5 silencing inhibits glucose uptake by 3T3-L1 adipocytes. These studies elucidate a previously unknown activity of Cdk5 and demonstrate the involvement of this kinase in the regulation of insulin-dependent glucose uptake in adipocytes.
摘要
在此，我们报告Cdk5的激活受胰岛素刺激，并在3T3-L1脂肪细胞中GLUT4介导的葡萄糖摄取调节中起关键作用。Cdk5的胰岛素激活需要PI3K信号传导。胰岛素激活的Cdk5使E-Syt1磷酸化，E-Syt1是一种与突触结合蛋白相关的含5个C2结构域的蛋白质，在脂肪细胞分化过程中被诱导产生。磷酸化的E-Syt1与GLUT4结合，这一事件被Cdk抑制剂roscovitine抑制。Cdk5沉默抑制3T3-L1脂肪细胞的葡萄糖摄取。这些研究阐明了Cdk5以前未知的活性，并证明了这种激酶参与脂肪细胞中胰岛素依赖性葡萄糖摄取的调节。
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