JNK regulates autocrine expression of TGF-β1

被引：78
|
作者：
Ventura, JJ
Kennedy, NJ
Flavell, RA
Davis, RJ [1 ]
机构：
[1] Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA
[2] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA
[3] Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA
[4] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA
来源：
MOLECULAR CELL | 2004年 / 15卷 / 02期
关键词：
D O I：
10.1016/j.molcel.2004.06.007
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：
The c-Jun NH2-terminal kinase (JNK) has been implicated in the function of transforming growth factor P (TGF-beta). To test the role of JNK, we examined the effect of compound disruption of the murine genes that encode the ubiquitously expressed isoforms of JNK (Jnk1 and Jnk2). We report that JNK-deficient fibroblasts isolated from Jnk1(-/-) Jnk2(-/-) mice constitutively express TGF-beta1. Complementation studies demonstrate that JNK is a repressor of Tgf-beta1 gene expression. This mechanism of regulation of TGF-beta1 expression by JNK represents an unexpected form of cross-talk between two important signaling pathways. Together, these data demonstrate that the JNK pathway may contribute to the regulation of autocrine TGF-beta1-mediated biological responses in vivo.
引用
收藏
页码：269 / 278
页数：10
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