Literature DB >> 15260977

JNK regulates autocrine expression of TGF-beta1.

Juan-Jose Ventura1, Norman J Kennedy, Richard A Flavell, Roger J Davis.   

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.

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Year:  2004        PMID： 15260977     DOI： 10.1016/j.molcel.2004.06.007

Source DB:  PubMed          Journal:  Mol Cell        ISSN： 1097-2765            Impact factor:   17.970


  28 in total

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