期刊
FEBS LETTERS
卷 582, 期 2, 页码 291-298出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2007.12.021
关键词
epithelial-mesenchymal transition; MRTF; epithelial injury; cell adhesion
资金
- Canadian Institutes of Health Research [75713] Funding Source: Medline
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) Rae, 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 Rae, PAK, and p38 in the regulation of MRTF and the contact-dependent induction of EMT. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据