Jing Wu, a postdoctoral fellow in Dr. Sigmund’s laboratory, has been awarded an Association-Wide Postdoctoral Fellowship (17POST33660685) from the American Heart Association for his project entitled “The Role of Endothelial Cullin3 in Vascular Function and Blood Pressure Regulation”. The goal of this project is to investigate the vascular mechanism in the pathogenesis of hypertension observed in human subjects with Cullin3 mutations. To do this, mice carrying a conditionally-activatable Cul3Δ9 transgene (lacking exon 9) will be crossed to tamoxifen-inducible Tie2-CRE mice to achieve endothelial-specific expression of this dominant negative Cul3 mutation. The resultant mice termed E-Cul3Δ9 exhibit vascular dysfunction, arterial stiffening, and nocturnal hypertension. Dr. Wu’s recent data demonstrate these phenotypes are caused by impaired Cullin3-mediated degradation of protein phosphatase 2A (PP2A), decreased phosphorylation of endothelial nitric oxide synthase (eNOS), and consequently decreased production of the vasodilatory nitric oxide molecule. These exciting results will be presented at the AHA Council on Hypertension 2017 Scientific Sessions held in San Francisco this September, where Dr. Wu will also receive a New Investigators Travel Award.