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Publication : JNK regulates autocrine expression of TGF-beta1.

First Author  Ventura JJ Year  2004
Journal  Mol Cell Volume  15
Issue  2 Pages  269-78
PubMed ID  15260977 Mgi Jnum  J:91462
Mgi Id  MGI:3047167 Doi  10.1016/j.molcel.2004.06.007
Citation  Ventura JJ, et al. (2004) JNK Regulates Autocrine Expression of TGF-beta1. Mol Cell 15(2):269-78
abstractText  The c-Jun NH(2)-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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