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II类磷酸肌醇3激酶C2α由网格蛋白激活,并调节网格蛋白介导的膜运输。

The class II phosphoinositide 3-kinase C2alpha is activated by clathrin and regulates clathrin-mediated membrane trafficking.

作者信息

Gaidarov I, Smith M E, Domin J, Keen J H

机构信息

Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.

出版信息

Mol Cell. 2001 Feb;7(2):443-9. doi: 10.1016/s1097-2765(01)00191-5.

Abstract

Phosphoinositides play key regulatory roles in vesicular transport pathways in eukaryotic cells. Clathrin-mediated membrane trafficking has been shown to require phosphoinositides, but little is known about the enzyme(s) responsible for their formation. Here we report that clathrin functions as an adaptor for the class II PI 3-kinase C2alpha (PI3K-C2alpha), binding to its N-terminal region and stimulating its catalytic activity, especially toward phosphorylated inositide substrates. Further, we show that endogenous PI3K-C2alpha is localized in coated pits and that exogenous expression affects clathrin-mediated endocytosis and sorting in the trans-Golgi network. These findings provide a mechanistic basis for localized inositide generation at sites of clathrin-coated bud formation, which, with recruitment of inositide binding proteins and subsequent synaptojanin-mediated phosphoinositide hydrolysis, may regulate coated vesicle formation and uncoating.

摘要

磷酸肌醇在真核细胞的囊泡运输途径中发挥关键的调节作用。网格蛋白介导的膜运输已被证明需要磷酸肌醇,但对于负责其形成的酶了解甚少。在此,我们报告网格蛋白作为II类PI 3激酶C2α(PI3K-C2α)的衔接蛋白,与其N端区域结合并刺激其催化活性,特别是对磷酸化肌醇底物的活性。此外,我们表明内源性PI3K-C2α定位于被膜小窝,并且外源性表达影响网格蛋白介导的内吞作用以及反式高尔基体网络中的分选。这些发现为网格蛋白包被芽形成位点处局部肌醇生成提供了机制基础,其与肌醇结合蛋白的募集以及随后突触素介导的磷酸肌醇水解一起,可能调节包被囊泡的形成和解包被。

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