TAB1: An activator of the TAK1 MAPKKK in TGF-beta signal transduction

被引：535
作者：
Shibuya, H
Yamaguchi, K
Shirakabe, K
Tonegawa, A
Gotoh, Y
Ueno, N
Irie, K
Nishida, E
Matsumoto, K
机构：
[1] NAGOYA UNIV, FAC SCI, DEPT MOLEC BIOL, CHIKUSA KU, NAGOYA, AICHI 46401, JAPAN
[2] RES DEV CORP JAPAN, PRECURSORY RES EMBRYON SCI & TECHNOL, HIKARI, KYOTO 61902, JAPAN
[3] HOKKAIDO UNIV, FAC PHARMACEUT SCI, SAPPORO, HOKKAIDO 060, JAPAN
[4] KYOTO UNIV, INST VIRUS RES, DEPT GENET & MOL BIOL, SAKYO KU, KYOTO 60601, JAPAN
来源：
SCIENCE | 1996年 / 272卷 / 5265期
关键词：
D O I：
10.1126/science.272.5265.1179
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Transforming growth factor-beta (TGF-B) regulates many aspects of cellular function. A member of the mitogen-activated protein kinase kinase kinase (MAPKKK) family, TAK1, was previously identified as a mediator in the signaling pathway of TGF-beta superfamily members. The yeast two-hybrid system has now revealed two human proteins, termed TAB1 and TAB2 (for TAK1 binding protein), that interact with TAK1. TAB1 and TAK1 were co-immunoprecipitated from mammalian cells. Overproduction of TAB1 enhanced activity of the plasminogen activator inhibitor 1 gene promoter, which is regulated by TGF-beta, and increased the kinase activity of TAK1. TAB1 may function as an activator of the TAK1 MAPKKK in TGF-beta signal transduction.
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收藏
页码：1179 / 1182
页数：4
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