Autoinhibition of Sos by intramolecular interactions

被引：11

作者：

Hall, BE

Yang, SS

Sagi, DB

机构：

[1] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA

[2] SUNY Stony Brook, Grad Programs Mol Pharmacol, Stony Brook, NY 11794 USA

[3] SUNY Stony Brook, Grad Programs Mol & Cellular Biol, Stony Brook, NY 11794 USA

来源：

FRONTIERS IN BIOSCIENCE | 2002年 / 7卷

关键词：

Ras; Sos; autoinhibition; receptor tyrosine kinase; guanine nucleotide exchange; intramolecular interaction; review;

D O I：

10.2741/hall

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Sos proteins function as activators of Ras signaling by catalyzing guanine nucleotide exchange on Ras. Sos regulation was initially thought to be accomplished primarily through its growth factor-dependent recruitment to the plasma membrane. More recent data has indicated that while membrane association is an indispensable means of Sos regulation, additional mechanisms involving intramolecular interactions function to control Sos activity towards Ras. This review will examine the experimental evidence for Sos intramolecular interactions and their contribution to Sos regulation.

引用

收藏

页码：D288 / D294

页数：7

相关论文

共 55 条

[41] N terminus of Sos1 Ras exchange factor: Critical roles for the Dbl and pleckstrin homology domains [J].

Qian, XL ;

Vass, WC ;

Papageorge, AG ;

Anborgh, PH ;

Lowy, DR .

MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (02) :771-778

[42]

ROZAKISADCOCK M, 1995, ONCOGENE, V11, P1417

[43] THE SH2 AND SH3 DOMAINS OF MAMMALIAN GRB2 COUPLE THE EGF RECEPTOR TO THE RAS ACTIVATOR MSOS1 [J].

ROZAKISADCOCK, M ;

FERNLEY, R ;

WADE, J ;

PAWSON, T ;

BOWTELL, D .

NATURE, 1993, 363 (6424) :83-85

[44] ASSOCIATION OF THE SHC AND GRB2/SEM5 SH2-CONTAINING PROTEINS IS IMPLICATED IN ACTIVATION OF THE RAS PATHWAY BY TYROSINE KINASES [J].

ROZAKISADCOCK, M ;

MCGLADE, J ;

MBAMALU, G ;

PELICCI, G ;

DALY, R ;

LI, W ;

BATZER, A ;

THOMAS, S ;

BRUGGE, J ;

PELICCI, PG ;

SCHLESSINGER, J ;

PAWSON, T .

NATURE, 1992, 360 (6405) :689-692

[45] ACTIVATION OF RAS AND OTHER SIGNALING PATHWAYS BY RECEPTOR TYROSINE KINASES [J].

SCHLESSINGER, J ;

BARSAGI, D .

COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY, 1994, 59 :173-179

[46] Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16(INK4a) [J].

Serrano, M ;

Lin, AW ;

McCurrach, ME ;

Beach, D ;

Lowe, SW .

CELL, 1997, 88 (05) :593-602

[47] GRB2 SH3 BINDING TO PEPTIDES FROM SOS - EVALUATION OF A GENERAL-MODEL FOR SH3-LIGAND INTERACTIONS [J].

SIMON, JA ;

SCHREIBER, SL .

CHEMISTRY & BIOLOGY, 1995, 2 (01) :53-60

[48] RAS1 AND A PUTATIVE GUANINE-NUCLEOTIDE EXCHANGE FACTOR PERFORM CRUCIAL STEPS IN SIGNALING BY THE SEVENLESS PROTEIN TYROSINE KINASE [J].

SIMON, MA ;

BOWTELL, DDL ;

DODSON, GS ;

LAVERTY, TR ;

RUBIN, GM .

CELL, 1991, 67 (04) :701-716

[49] THE SH2 SH3 DOMAIN-CONTAINING PROTEIN GRB2 INTERACTS WITH TYROSINE-PHOSPHORYLATED IRS1 AND SHC - IMPLICATIONS FOR INSULIN CONTROL OF RAS SIGNALING [J].

SKOLNIK, EY ;

LEE, CH ;

BATZER, A ;

VICENTINI, LM ;

ZHOU, M ;

DALY, R ;

MYERS, MJ ;

BACKER, JM ;

ULLRICH, A ;

WHITE, MF ;

SCHLESSINGER, J .

EMBO JOURNAL, 1993, 12 (05) :1929-1936

[50] Crystal structure of the Dbl and pleckstrin homology domains from the human Son of Sevenless protein [J].

Soisson, SM ;

Nimnual, AS ;

Uy, M ;

Bar-Sagi, D ;

Kuriyan, J .

CELL, 1998, 95 (02) :259-268

← 1 2 3 4 5 6 →