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MRC Human Genetics Unit and Institute f... Publications | LitMetric

3 results match your criteria: "MRC Human Genetics Unit and Institute for Genetics and Molecular Medicine[Affiliation]"

WT1 in disease: shifting the epithelial-mesenchymal balance.

J Pathol

January 2012

MRC Human Genetics Unit and Institute for Genetics and Molecular Medicine, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK.

WT1 is a versatile gene that controls transitions between the mesenchymal and epithelial state of cells in a tissue-context dependent manner. As such, WT1 is indispensable for normal development of many organs and tissues. Uncontrolled epithelial to mesenchymal transition (EMT) is a hallmark of a diverse array of pathologies and disturbance of mesenchymal to epithelial transition (MET) has been associated with a number of developmental abnormalities.

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A wt1-controlled chromatin switching mechanism underpins tissue-specific wnt4 activation and repression.

Dev Cell

September 2011

MRC Human Genetics Unit and Institute for Genetics and Molecular Medicine, Western General Hospital, Edinburgh EH4 2XU, UK.

Wt1 regulates the epithelial-mesenchymal transition (EMT) in the epicardium and the reverse process (MET) in kidney mesenchyme. The mechanisms underlying these reciprocal functions are unknown. Here, we show in both embryos and cultured cells that Wt1 regulates Wnt4 expression dichotomously.

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The epicardial epithelial-mesenchymal transition (EMT) is hypothesized to generate cardiovascular progenitor cells that differentiate into various cell types, including coronary smooth muscle and endothelial cells, perivascular and cardiac interstitial fibroblasts and cardiomyocytes. Here we show that an epicardial-specific knockout of the gene encoding Wilms' tumor-1 (Wt1) leads to a reduction in mesenchymal progenitor cells and their derivatives. We show that Wt1 is essential for repression of the epithelial phenotype in epicardial cells and during embryonic stem cell differentiation through direct transcriptional regulation of the genes encoding Snail (Snai1) and E-cadherin (Cdh1), two of the major mediators of EMT.

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