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Publication : Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis.

First Author  Vijayaraj P Year  2012
Journal  Development Volume  139
Issue  21 Pages  3973-85
PubMed ID  22932696 Mgi Jnum  J:188920
Mgi Id  MGI:5442628 Doi  10.1242/dev.081596
Citation  Vijayaraj P, et al. (2012) Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis. Development 139(21):3973-85
abstractText  During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells of the developing vasculature and in articular chondrocytes of developing bone. We identified seven isoforms for the mouse Erg gene. Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes. The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells. Homozygous Erg(DeltaEx3/DeltaEx3) knockout mice are viable, fertile and do not display any overt phenotype. By contrast, homozygous Erg(DeltaEx4/DeltaEx4) knockout mice are embryonic lethal, which is associated with a marked reduction in endocardial-mesenchymal transformation (EnMT) during cardiac valve morphogenesis. We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.
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