I am a Professor of Internal Medicine in the Division of Cardiology at UT Southwestern Medical Center and also serve as acting chair for the Therapeutic Approaches to Genetic Disease (TAG) study section at NIH.  My expertise is in molecular biology/biochemistry with a focus on intracellular signaling, metabolism, and autophagy.  My laboratory studies the mechanisms that mediate remodeling of the cardiovascular and skeletal muscle systems during development and disease.  Central to many of our studies is the protein RCAN1/DSCR1, encoded on chromosome 21 in humans. I was among the first to identify RCAN1 as a feedback inhibitor of the Ca²⁺-activated protein phosphatase calcineurin.  Experiments in my lab have sought to better understand the biochemistry of the RCAN1/calcineurin interaction, identify transcriptional and post-transcriptional mechanisms controlling RCAN1, and determine the physiological consequences of RCAN1 regulation in the heart and other organs. I have had a long-standing interest in the potential impact of the RCAN1/DSCR1 locus on the pathophysiology of Down syndrome (DS).  Studies from my laboratory have revealed important connections between changes in RCAN1 gene dosage and metabolic control.  We’ve shown that mitochondria in induced pluripotent stem cells (iPSCs) derived from DS patients are hyperfused with elevated metabolic activity, and that reducing RCAN1 levels alone is sufficient to restore normal stem cell metabolism.  We have evidence that this fundamental difference in stem cell metabolism negatively impacts the ability of DS stem cells to differentiate toward a neuronal lineage.  My approach to science is highly collaborative and this has provided many opportunities to integrate work in my laboratory with that of researchers in many other fields, yielding important insights into the diverse functions of RCAN1 and its contributions to DS pathologies.