EEA1 links PI(3)K function to Rab5 regulation of endosome fusion.

来自 Springer

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作者：

Simonsen,A，Lippe,R，Christoforidis,S，Gaullier,JM，Brech,A，Callaghan,J，Toh,BH，Murphy,C，Zerial,M，Stenmark,H

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摘要：

GTPases and lipid kinases regulate membrane traffic along the endocytic pathway by mechanisms that are not completely understood. Fusion between early endosomes requires phosphatidylinositol-3-OH kinase (PI(3)K) activity as well as the small GTPase Rab5. Excess Rab5-GTP complex restores endosome fusion when PI(3)K is inhibited. Here we identify the early-endosomal autoantigen EEA1 which binds the PI(3)K product phosphatidylinositol-3-phosphate, as a new Rab5 effector that is required for endosome fusion. The association of EEA1 with the endosomal membrane requires Rab5-GTP and PI(3)K activity, and excess Rab5-GTP stabilizes the membrane association of EEA1 even when PI(3)K is inhibited. The identification of EEA1 as a direct Rab5 effector provides a molecular link between PI(3)K and Rab5, and its restricted distribution to early endosomes indicates that EEA1 may confer directionality to Rab5-dependent endocytic transport.

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关键词：

Endosomes GTP-Binding Proteins Membrane Fusion Membrane Proteins 1-Phosphatidylinositol 3-Kinase 内颗粒 GTP-结合蛋白质类膜融合膜蛋白质类 1-磷脂酰肌醇3-激酶