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| Research article summary (published 13 Nov 2002): |
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Syndapins integrate N-WASP in receptor-mediated endocytosis.
Full Abstract
Syndapins are potential links between the cortical actin cytoskeleton and endocytosis because this family of dynamin-associated proteins can also interact with the Arp2/3 complex activator N-WASP. Here we provide evidence for involvement of N-WASP interactions in receptor-mediated endocytosis. We reveal that the observed dominant-negative effects of N-WASP are dependent exclusively on the proline-rich domain, the binding interface of syndapins. Our results therefore suggest that syndapins integrate N-WASP functions in endocytosis. Both proteins co-localize in neuronal cells. Consistent with a crucial role for syndapins in endocytic uptake, co-overexpression of syndapins rescued the endocytosis block caused by N-WASP. An in vivo reconstitution of the syndapin-N-WASP interaction at cellular membranes triggered local actin polymerization. Depletion of endogenous N-WASP by sequestering it to mitochondria or by introducing anti-N-WASP antibodies impaired endocytosis. Our data suggest that syndapins may act as important coordinators of N-WASP and dynamin functions during the different steps of receptor-mediated endocytosis and that local actin polymerization induced by syndapin-N-WASP interactions may be a mechanism supporting clathrin-coated vesicle detachment and movement away from the plasma membrane.
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Author information
Author/s: Kessels, Michael M (MM); Qualmann, Britta (B);
Affiliation: Department of Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology, Brenneckestrasse 6, D-39118 Magdeburg, Germany.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: The EMBO journal (EMBO J), published in England. (Language: eng)
Reference: 2002-Nov; vol 21 (issue 22) : pp 6083-94
Dates: Created 2002/11/11; Completed 2003/01/02; Revised 2006/11/15;
PMID: 12426380, status: MEDLINE (last retrieval date: 11/6/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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