Research Abstract

My research program focuses on the fundamental mechanisms underlying both congenital heart disease and end-stage heart failure, and the mechanisms therein that lead to abnormal development, aberrant molecular signaling, and disease onset. Our lab uses a myriad of tools and techniques including iPS cells, in vivo mouse model systems, and molecular biology techniques. Together, these provide valuable mechanistic and functional information in understanding the differential signaling pathways and developmental processes leading to cardiac disease. Our lab has three main interests: 1) elucidation of the cardiomyogenic defects associated with Noonan and LEOPARD Syndromes, two autosomal dominant congenital disorders primarily caused by unique mutations in the protein tyrosine phosphatase Shp2; 2) understanding the functional role and mechanisms by which Shp2 activity is involved in the development of Systemic Lupus Erythematosus; and 3) elucidating the potential cardioprotective effects of the small G protein RhoA in the adult heart through identification of novel signaling pathways involved in cardiac pathogenesis.