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Mol Cell. 2004 Jul 23;15(2):269-78.

JNK regulates autocrine expression of TGF-beta1.

Author information

1
Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester 01605, USA.

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.

PMID:
15260977
DOI:
10.1016/j.molcel.2004.06.007
[Indexed for MEDLINE]
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