Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism

The small GTPase Arf6 regulates intracellular transport, phosphoinositide signalling and cholesterol homeostasis. Here, Marquer et al. show that loss of Arf6 causes cholesterol accumulation in endosomes due to defects in phosphoinositide-dependent retromer-mediated trafficking of CI-M6PR and NPC2.

Bibliographic Details
Main Authors:	Catherine Marquer, Huasong Tian, Julie Yi, Jayson Bastien, Claudia Dall'Armi, YoungJoo Yang-Klingler, Bowen Zhou, Robin Barry Chan, Gilbert Di Paolo
Format:	Article
Language:	English
Published:	Nature Publishing Group 2016-06-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/ncomms11919

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spelling	doaj-2c2430c3a2ba4bf78869ca4b08f032c72021-05-11T11:23:16ZengNature Publishing GroupNature Communications2041-17232016-06-017111410.1038/ncomms11919Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanismCatherine Marquer0Huasong Tian1Julie Yi2Jayson Bastien3Claudia Dall'Armi4YoungJoo Yang-Klingler5Bowen Zhou6Robin Barry Chan7Gilbert Di Paolo8Department of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterDepartment of Pathology and Cell Biology, Columbia University Medical CenterThe small GTPase Arf6 regulates intracellular transport, phosphoinositide signalling and cholesterol homeostasis. Here, Marquer et al. show that loss of Arf6 causes cholesterol accumulation in endosomes due to defects in phosphoinositide-dependent retromer-mediated trafficking of CI-M6PR and NPC2.https://doi.org/10.1038/ncomms11919
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Catherine Marquer Huasong Tian Julie Yi Jayson Bastien Claudia Dall'Armi YoungJoo Yang-Klingler Bowen Zhou Robin Barry Chan Gilbert Di Paolo
spellingShingle	Catherine Marquer Huasong Tian Julie Yi Jayson Bastien Claudia Dall'Armi YoungJoo Yang-Klingler Bowen Zhou Robin Barry Chan Gilbert Di Paolo Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism Nature Communications
author_facet	Catherine Marquer Huasong Tian Julie Yi Jayson Bastien Claudia Dall'Armi YoungJoo Yang-Klingler Bowen Zhou Robin Barry Chan Gilbert Di Paolo
author_sort	Catherine Marquer
title	Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism
title_short	Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism
title_full	Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism
title_fullStr	Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism
title_full_unstemmed	Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism
title_sort	arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2016-06-01
description	The small GTPase Arf6 regulates intracellular transport, phosphoinositide signalling and cholesterol homeostasis. Here, Marquer et al. show that loss of Arf6 causes cholesterol accumulation in endosomes due to defects in phosphoinositide-dependent retromer-mediated trafficking of CI-M6PR and NPC2.
url	https://doi.org/10.1038/ncomms11919
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Arf6 controls retromer traffic and intracellular cholesterol distribution via a phosphoinositide-based mechanism

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