EEA1 links PI(3)K function to Rab5 regulation of endosome fusion - PubMed (original) (raw)
. 1998 Jul 30;394(6692):494-8.
doi: 10.1038/28879.
Affiliations
- PMID: 9697774
- DOI: 10.1038/28879
EEA1 links PI(3)K function to Rab5 regulation of endosome fusion
A Simonsen et al. Nature. 1998.
Abstract
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.
Comment in
- Vesicular transport. Sticky fingers grab a lipid.
Wiedemann C, Cockcroft S. Wiedemann C, et al. Nature. 1998 Jul 30;394(6692):426-7. doi: 10.1038/28752. Nature. 1998. PMID: 9697761 No abstract available.
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