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FEBS Lett. 2008 Jan 23;582(2):291-8. Epub 2007 Dec 27.

Rac, PAK and p38 regulate cell contact-dependent nuclear translocation of myocardin-related transcription factor.

Author information

1
Keenan Research Centre, Li Ka Shing Knowledge Institute of St. Michael's Hospital, 30 Bond Street, Toronto, Ontario, Canada.

Abstract

We investigated the mechanism whereby cell contact injury stimulates the alpha-smooth muscle actin (SMA) promoter, a key process for epithelial-mesenchymal transition (EMT) during organ fibrosis. Contact disruption by low-Ca(2+) medium (LCM) activated Rac, PAK and p38 MAPK, and triggered the nuclear accumulation of myocardin-related transcription factor (MRTF), an inducer of the SMA promoter. Dominant negative (DN) Rac, DN-PAK, DN-p38, or the p38 inhibitor SB203580 suppressed the LCM-induced nuclear accumulation of MRTF and the activation of the SMA promoter. These studies define novel pathway(s) involving Rac, PAK, and p38 in the regulation of MRTF and the contact-dependent induction of EMT.

PMID:
18154735
PMCID:
PMC5047756
DOI:
10.1016/j.febslet.2007.12.021
[Indexed for MEDLINE]
Free PMC Article

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