Activation of apoptosis signal regulating kinase 1 (ASK1) by the adapter protein Daxx

被引：514

作者：

Chang, HY

Nishitoh, H

Yang, XL

Ichijo, H

Baltimore, D

机构：

[1] Tokyo Med & Dent Univ, Fac Dent, Dept Biomat Sci, Bunkyo Ku, Tokyo 1138549, Japan

[2] MIT, Dept Biol, Cambridge, MA 02138 USA

[3] Japanese Fdn Canc Res, Inst Canc, Dept Biochem, Toshima Ku, Tokyo 170, Japan

[4] CALTECH, Pasadena, CA 91125 USA

来源：

SCIENCE | 1998年 / 281卷 / 5384期

关键词：

D O I：

10.1126/science.281.5384.1860

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：

The Fas death receptor can activate the Jun NH2-terminal kinase (JNK) pathway through the receptor-associated protein Daxx. Daxx was found to activate the JNK kinase kinase ASK1, and overexpression of a kinase-deficient ASK1 mutant inhibited Fas- and Daxx-induced apoptosis and JNK activation. Fas activation induced Daxx to interact with ASK1, which consequently relieved an inhibitory intramolecular interaction between the amino- and carboxyl-termini of ASK1, activating its kinase activity. The Daxx-ASK1 connection completes a signaling pathway from a cell surface death receptor to kinase cascades that modulate nuclear transcription factors.

引用

页码：1860 / 1863

页数：4

共 22 条

[21] FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis [J].