An ACAP1-containing clathrin coat complex for endocytic recycling

被引：91

作者：

Li, Jian

Peters, Peter J.

Bai, Ming

Dai, Jun

Bos, Erik

Kirchhausen, Tomas

Kandror, Konstantin V.

Hsu, Victor W. ^{[1
]}

机构：

[1] Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA

[4] Harvard Univ, Sch Med, DBR Inst Biomed Res, Boston, MA 02115 USA

[5] Netherlands Canc Inst, Div Cell Biol, NL-1066 CX Amsterdam, Netherlands

[6] Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA

来源：

JOURNAL OF CELL BIOLOGY | 2007年 / 178卷 / 03期

关键词：

D O I：

10.1083/jcb.200608033

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：453 / 464

页数：12

共 44 条

[1] The KDEL receptor, ERD2, regulates intracellular traffic by recruiting a GTPase-activating protein for ARF1 [J].