Mouse Models of Human Conotruncal Defects

$271,357P01FY2014HDNIH

Albert Einstein College Of Medicine, Bronx NY

Investigators

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Abstract

We will determine the molecular pathogenesis of CTDs by taking mouse genetics approaches. We propose that Tbxl genetic pathways are required for cardiac outflow tract development and when altered alters risk to CTDs in 22q11DS (Project 1) and more frequent non-syndromic forms (Project 2).

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