EEA1 links PI(3)K function to Rab5 regulation of endosome fusion
dc.contributor.author | Simonsen, A. | en |
dc.contributor.author | Lippe, R. | en |
dc.contributor.author | Christoforidis, S. | en |
dc.contributor.author | Gaullier, J. M. | en |
dc.contributor.author | Brech, A. | en |
dc.contributor.author | Callaghan, J. | en |
dc.contributor.author | Toh, B. H. | en |
dc.contributor.author | Murphy, C. | en |
dc.contributor.author | Zerial, M. | en |
dc.contributor.author | Stenmark, H. | en |
dc.date.accessioned | 2015-11-24T19:23:09Z | |
dc.date.available | 2015-11-24T19:23:09Z | |
dc.identifier.issn | 0028-0836 | - |
dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/22258 | |
dc.rights | Default Licence | - |
dc.subject | Androstadienes/pharmacology | en |
dc.subject | Animals | en |
dc.subject | Autoantigens/physiology | en |
dc.subject | Cattle | en |
dc.subject | Cell Line | en |
dc.subject | Cloning, Molecular | en |
dc.subject | Cricetinae | en |
dc.subject | Endosomes/*physiology | en |
dc.subject | Enzyme Inhibitors/pharmacology | en |
dc.subject | GTP-Binding Proteins/genetics/*physiology | en |
dc.subject | Guanosine Triphosphate/physiology | en |
dc.subject | HeLa Cells | en |
dc.subject | Humans | en |
dc.subject | Intracellular Membranes/physiology | en |
dc.subject | Membrane Fusion/*physiology | en |
dc.subject | Membrane Proteins/genetics/*physiology | en |
dc.subject | Mutagenesis | en |
dc.subject | Phosphatidylinositol 3-Kinases/antagonists & inhibitors/*physiology | en |
dc.subject | Recombinant Fusion Proteins/metabolism | en |
dc.subject | Vesicular Transport Proteins | en |
dc.subject | rab5 GTP-Binding Proteins | en |
dc.title | EEA1 links PI(3)K function to Rab5 regulation of endosome fusion | en |
heal.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. | en |
heal.access | campus | - |
heal.fullTextAvailability | TRUE | - |
heal.identifier.primary | 10.1038/28879 | - |
heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/9697774 | - |
heal.journalName | Nature | en |
heal.journalType | peer-reviewed | - |
heal.language | en | - |
heal.publicationDate | 1998 | - |
heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
heal.type | journalArticle | - |
heal.type.el | Άρθρο Περιοδικού | el |
heal.type.en | Journal article | en |
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