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pubmed-article:20016221pubmed:abstractTextEpithelial-mesenchymal transition of tubular cells into alpha-smooth muscle actin (SMA)-expressing myofibroblasts is a central mechanism in tubulointerstitial fibrosis. Previously, a 'two-hit' model was proposed for epithelial-mesenchymal transition wherein an initial injury of the intercellular contacts and TGF-beta(1) are both required for SMA protein expression in LLC-PK1 cells. The Rho-Rho kinase-myosin light chain-myocardin-related transcription factor (MRTF)-serum response factor (SRF) pathway and Rac1, p21-activated kinase (PAK) and p38 were described as important regulators of MRTF localization and SMA expression. Cdc42 is another small G protein situated upstream of PAK and p38, and is activated upon cell contact disassembly. Here, we investigated its potential role in the regulation of MRTF nuclear shuttling and in the regulation of the SMA promoter.lld:pubmed
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pubmed-article:20016221pubmed:articleTitleCdc42 regulates myocardin-related transcription factor nuclear shuttling and alpha-smooth muscle actin promoter activity during renal tubular epithelial-mesenchymal transition.lld:pubmed
pubmed-article:20016221pubmed:affiliationDepartment of Pathophysiology, Semmelweis University and Pediatrics and Nephrology Research Group, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary.lld:pubmed
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