JNK调节转化生长因子β1（TGF-beta1）的自分泌表达。

JNK regulates autocrine expression of TGF-beta1.

作者信息

Ventura Juan-Jose, Kennedy Norman J, Flavell Richard A, Davis Roger J

机构信息

Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester 01605, USA.

出版信息

Mol Cell. 2004 Jul 23;15(2):269-78. doi: 10.1016/j.molcel.2004.06.007.

DOI:10.1016/j.molcel.2004.06.007

PMID:15260977

Abstract

The c-Jun NH2-terminal kinase (JNK) has been implicated in the function of transforming growth factor beta (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.

摘要

c-Jun氨基末端激酶（JNK）与转化生长因子β（TGF-β）的功能有关。为了测试JNK的作用，我们研究了编码普遍表达的JNK亚型（Jnk1和Jnk2）的小鼠基因复合破坏的影响。我们报告说，从Jnk1-/-Jnk2-/-小鼠分离的JNK缺陷型成纤维细胞组成性表达TGF-β1。互补研究表明，JNK是Tgf-β1基因表达的抑制因子。JNK对TGF-β1表达的这种调节机制代表了两条重要信号通路之间一种意想不到的相互作用形式。总之，这些数据表明JNK通路可能有助于体内自分泌TGF-β1介导的生物学反应的调节。