ACAP1 promotes endocytic recycling - Short article by recognizing recycling sorting signals

被引：91

作者：

Dai, J

Li, J

Bos, E

Porcionatto, M

Premont, RT

Bourgoin, S

Peters, PJ

Hsu, VW ^{[1
]}

机构：

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

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

[3] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA

[4] Univ Quebec, Ctr Hosp, CHUL, Pavillion Rhumatol & Immunol, Quebec City, PQ G1V 4G2, Canada

[5] Duke Univ, Ctr Med, Div Gastroenterol, Dept Pediat Oncol, Durham, NC 27710 USA

来源：

DEVELOPMENTAL CELL | 2004年 / 7卷 / 05期

基金：

加拿大健康研究院; 美国国家卫生研究院;

关键词：

D O I：

10.1016/j.devcel.2004.10.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cargo sorting that promotes the transport of cargo proteins from a membrane compartment has been predicted to be unlikely in the endocytic recycling pathways. We now show that ACAP1 binds specifically and directly to recycling cargo proteins. Reducing this interaction for TfR inhibits its recycling. Moreover, ACAP1 binds to two distinct phenylalanine-based sequences in the cytoplasmic domain of TfR that function as recycling sorting signals to promote its transport from the recycling endosome. Taken together, these findings indicate that ACAP1 promotes cargo sorting by recognizing recycling sorting signals.

引用

页码：771 / 776

页数：6

共 22 条

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