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. 2016 Feb 1;27(3):535–548. doi: 10.1091/mbc.E15-06-0453

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© 2016 Patnaik, George, et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 7: — Working model for the role of villin in EMT. We suggest that in response to receptor activation (R), villin is tyrosine phosphorylated and trafficked into the nucleus. In the nucleus, villin interacts with the transcriptional cofactor ZBRK1, which prevents the interaction of ZBRK1 with Slug. Disruption of the ZBRK1-Slug interaction results in the activation and expression of the transcriptional factor Slug. This, we suggest, regulates EMT. The role of ZBRK1 in the regulation of Slug remains to be characterized. We hypothesize that nonreceptor tyrosine kinases and tyrosine phosphatases regulate the cytoplasmic–nuclear shuttling of villin in epithelial cells.