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An ACAP1-containing clathrin coat complex for endocytic recycling

Whether coat proteins play a widespread role in endocytic recycling remains unclear. We find that ACAP1, a GTPase-activating protein (GAP) for ADP-ribosylation factor (ARF) 6, is part of a novel clathrin coat complex that is regulated by ARF6 for endocytic recycling in two key physiological settings...

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Detalles Bibliográficos
Autores principales: Li, Jian, Peters, Peter J., Bai, Ming, Dai, Jun, Bos, Erik, Kirchhausen, Tomas, Kandror, Konstantin V., Hsu, Victor W.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064835/
https://www.ncbi.nlm.nih.gov/pubmed/17664335
http://dx.doi.org/10.1083/jcb.200608033
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author Li, Jian
Peters, Peter J.
Bai, Ming
Dai, Jun
Bos, Erik
Kirchhausen, Tomas
Kandror, Konstantin V.
Hsu, Victor W.
author_facet Li, Jian
Peters, Peter J.
Bai, Ming
Dai, Jun
Bos, Erik
Kirchhausen, Tomas
Kandror, Konstantin V.
Hsu, Victor W.
author_sort Li, Jian
collection PubMed
description Whether coat proteins play a widespread role in endocytic recycling remains unclear. We find that ACAP1, a GTPase-activating protein (GAP) for ADP-ribosylation factor (ARF) 6, is part of a novel clathrin coat complex that is regulated by ARF6 for endocytic recycling in two key physiological settings, stimulation-dependent recycling of integrin that is critical for cell migration and insulin-stimulated recycling of glucose transporter type 4 (Glut4), which is required for glucose homeostasis. These findings not only advance a basic understanding of an early mechanistic step in endocytic recycling but also shed key mechanistic insights into major physiological events for which this transport plays a critical role.
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spelling pubmed-20648352008-01-30 An ACAP1-containing clathrin coat complex for endocytic recycling Li, Jian Peters, Peter J. Bai, Ming Dai, Jun Bos, Erik Kirchhausen, Tomas Kandror, Konstantin V. Hsu, Victor W. J Cell Biol Research Articles Whether coat proteins play a widespread role in endocytic recycling remains unclear. We find that ACAP1, a GTPase-activating protein (GAP) for ADP-ribosylation factor (ARF) 6, is part of a novel clathrin coat complex that is regulated by ARF6 for endocytic recycling in two key physiological settings, stimulation-dependent recycling of integrin that is critical for cell migration and insulin-stimulated recycling of glucose transporter type 4 (Glut4), which is required for glucose homeostasis. These findings not only advance a basic understanding of an early mechanistic step in endocytic recycling but also shed key mechanistic insights into major physiological events for which this transport plays a critical role. The Rockefeller University Press 2007-07-30 /pmc/articles/PMC2064835/ /pubmed/17664335 http://dx.doi.org/10.1083/jcb.200608033 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Research Articles
Li, Jian
Peters, Peter J.
Bai, Ming
Dai, Jun
Bos, Erik
Kirchhausen, Tomas
Kandror, Konstantin V.
Hsu, Victor W.
An ACAP1-containing clathrin coat complex for endocytic recycling
title An ACAP1-containing clathrin coat complex for endocytic recycling
title_full An ACAP1-containing clathrin coat complex for endocytic recycling
title_fullStr An ACAP1-containing clathrin coat complex for endocytic recycling
title_full_unstemmed An ACAP1-containing clathrin coat complex for endocytic recycling
title_short An ACAP1-containing clathrin coat complex for endocytic recycling
title_sort acap1-containing clathrin coat complex for endocytic recycling
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064835/
https://www.ncbi.nlm.nih.gov/pubmed/17664335
http://dx.doi.org/10.1083/jcb.200608033
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