ARFGAP1 promotes AP-2-dependent endocytosis

被引:30
作者
Bai, Ming [1 ,2 ]
Gad, Helge [3 ,4 ]
Turacchio, Gabriele [3 ,5 ]
Cocucci, Emanuele [6 ,7 ]
Yang, Jia-Shu [1 ,2 ]
Li, Jian [1 ,2 ]
Beznoussenko, Galina V. [3 ]
Nie, Zhongzhen [8 ]
Luo, Ruibai [9 ]
Fu, Lianwu [10 ]
Collawn, James F. [10 ]
Kirchhausen, Tomas [6 ,7 ]
Luini, Alberto [3 ,11 ]
Hsu, Victor W. [1 ,2 ]
机构
[1] Harvard Univ, Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Sch Med, Boston, MA 02115 USA
[2] Harvard Univ, Dept Med, Sch Med, Boston, MA 02115 USA
[3] Ist Ric Farmacol Mario Negri, Consorzio Mario Negri Sud, Dept Cell Biol & Oncol, I-66030 Chieti, Italy
[4] Stockholm Univ, Dept Genet Microbiol & Toxicol, S-10691 Stockholm, Sweden
[5] CNR, Inst Prot Biochem, I-80131 Naples, Italy
[6] Harvard Univ, Dept Cell Biol, Sch Med, Boston, MA 02115 USA
[7] Immune Dis Inst, Boston, MA 02115 USA
[8] Univ Florida Coll Med, Dept Urol, Gainesville, FL 32610 USA
[9] NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA
[10] Univ Alabama, Dept Cell Biol, Birmingham, AL 35294 USA
[11] Telethon Inst Genet & Med, I-80131 Naples, Italy
基金
美国国家卫生研究院;
关键词
TRANSMEMBRANE CONDUCTANCE REGULATOR; CLATHRIN-MEDIATED ENDOCYTOSIS; COPI VESICLE FORMATION; TRANSFERRIN RECEPTOR; SORTING SIGNALS; GOLGI TRANSPORT; ENDOPLASMIC-RETICULUM; ADAPTER COMPLEX; ALPHA-APPENDAGE; COATED VESICLES;
D O I
10.1038/ncb2221
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
COPI (coat protein I) and the clathrin-AP-2 (adaptor protein 2) complex are well-characterized coat proteins, but a component that is common to these two coats has not been identified. The GTPase-activating protein (GAP) for ADP-ribosylation factor 1 (ARF1), ARFGAP1, is a known component of the COPI complex. Here, we show that distinct regions of ARFGAP1 interact with AP-2 and coatomer (components of the COPI complex). Selectively disrupting the interaction of ARFGAP1 with either of these two coat proteins leads to selective inhibition in the corresponding transport pathway. The role of ARFGAP1 in AP-2-regulated endocytosis has mechanistic parallels with its roles in COPI transport, as both its GAP activity and coat function contribute to promoting AP-2 transport.
引用
收藏
页码:559 / U144
页数:20
相关论文
共 58 条
[1]
INTERMOLECULAR DISULFIDE BONDS ARE NOT REQUIRED FOR THE EXPRESSION OF THE DIMERIC STATE AND FUNCTIONAL-ACTIVITY OF THE TRANSFERRIN RECEPTOR [J].
ALVAREZ, E ;
GIRONES, N ;
DAVIS, RJ .
EMBO JOURNAL, 1989, 8 (08) :2231-2240
[2]
COPII - A MEMBRANE COAT FORMED BY SEC PROTEINS THAT DRIVE VESICLE BUDDING FROM THE ENDOPLASMIC-RETICULUM [J].
BARLOWE, C ;
ORCI, L ;
YEUNG, T ;
HOSOBUCHI, M ;
HAMAMOTO, S ;
SALAMA, N ;
REXACH, MF ;
RAVAZZOLA, M ;
AMHERDT, M ;
SCHEKMAN, R .
CELL, 1994, 77 (06) :895-907
[3]
CtBP3/BARS drives membrane fission in dynamin-independent transport pathways [J].
Bonazzi, M ;
Spanò, S ;
Turacchio, G ;
Cericola, C ;
Valente, C ;
Colanzi, A ;
Kweon, HS ;
Hsu, VW ;
Polishchuck, EV ;
Polishchuck, RS ;
Sallese, M ;
Pulvirenti, T ;
Corda, D ;
Luini, A .
NATURE CELL BIOLOGY, 2005, 7 (06) :570-U11
[4]
The mechanisms of vesicle budding and fusion [J].
Bonifacino, JS ;
Glick, BS .
CELL, 2004, 116 (02) :153-166
[5]
Roles of AP-2 in Clathrin-Mediated Endocytosis [J].
Boucrot, Emmanuel ;
Saffarian, Saveez ;
Zhang, Rongying ;
Kirchhausen, Tomas .
PLOS ONE, 2010, 5 (05)
[6]
Coats, tethers, Rabs, and SNAREs work together to mediate the intracellular destination of a transport vesicle [J].
Cai, Huaqing ;
Reinisch, Karin ;
Ferro-Novick, Susan .
DEVELOPMENTAL CELL, 2007, 12 (05) :671-682
[7]
Regulation of arf activation: the sec7 family of guanine nucleotide exchange factors [J].
Casanova, James E. .
TRAFFIC, 2007, 8 (11) :1476-1485
[8]
Assays and properties of the Arf GAPs AGAP1, ASAP1, and Arf GAP1 [J].
Che, MM ;
Nie, ZZ ;
Randazzo, PA .
GTPASES REGULATING MEMBRANE DYNAMICS, 2005, 404 :147-163
[9]
Retrograde transport of Golgi-localized proteins to the ER [J].
Cole, NB ;
Ellenberg, J ;
Song, J ;
DiEuliis, D ;
Lippincott-Schwartz, J .
JOURNAL OF CELL BIOLOGY, 1998, 140 (01) :1-15
[10]
TRANSFERRIN RECEPTOR INTERNALIZATION SEQUENCE YXRF IMPLICATES A TIGHT TURN AS THE STRUCTURAL RECOGNITION MOTIF FOR ENDOCYTOSIS [J].
COLLAWN, JF ;
STANGEL, M ;
KUHN, LA ;
ESEKOGWU, V ;
JING, SQ ;
TROWBRIDGE, IS ;
TAINER, JA .
CELL, 1990, 63 (05) :1061-1072