Literature DB >> 18154735

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

Attila Sebe1, András Masszi, Matthew Zulys, Tony Yeung, Pam Speight, Ori D Rotstein, Hiroyasu Nakano, István Mucsi, Katalin Szászi, András Kapus.   

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.

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Year:  2007        PMID： 18154735      PMCID： PMC5047756          DOI： 10.1016/j.febslet.2007.12.021

Source DB:  PubMed          Journal:  FEBS Lett        ISSN： 0014-5793            Impact factor:   4.124


  28 in total

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Authors:  S Zhang; J Han; M A Sells; J Chernoff; U G Knaus; R J Ulevitch; G M Bokoch
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Review 9.  The epithelial-mesenchymal transition: new insights in signaling, development, and disease.

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  36 in total

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5.  Hyperosmotic stress induces Rho/Rho kinase/LIM kinase-mediated cofilin phosphorylation in tubular cells: key role in the osmotically triggered F-actin response.

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6.  TGF-β1 regulates the expression and transcriptional activity of TAZ protein via a Smad3-independent, myocardin-related transcription factor-mediated mechanism.

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7.  Hyperosmotic stress regulates the distribution and stability of myocardin-related transcription factor, a key modulator of the cytoskeleton.

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8.  Induction of megakaryocyte differentiation drives nuclear accumulation and transcriptional function of MKL1 via actin polymerization and RhoA activation.

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9.  Fate-determining mechanisms in epithelial-myofibroblast transition: major inhibitory role for Smad3.

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10.  Carbon monoxide modulates alpha-smooth muscle actin and small proline rich-1a expression in fibrosis.

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