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Figure 8


Fig. 8. Model of the regulation of MAL/SRF-dependent transcription by epithelial junctions. Disassembly of E-cadherin-mediated cell-cell contacts leads to transient activation of Rac and alterations in actin treadmilling. This releases the G-actin-mediated inhibition of MAL. GTP-loaded Rac is both required and sufficient for MAL and SRF activation upon epithelial disintegration, and subsequent transcription of endogenous target genes such as vinculin (vcl) and smooth muscle {alpha}-actin (acta2). Actomyosin contractility is a prerequisite for appropriate actin remodelling during this process. Blue bars represent transmembrane proteins.





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