Dr. Keytam S. Awad was trained as a cellular and molecular biologist and received her PhD from Kent State University in Ohio. There she studied the mechanisms by which natural ligands suppress viral oncogene function as a novel approach to inhibit human papillomavirus-induced precancerous and cancerous lesions. Dr. Awad joined the NIH Critical Care Medicine Department as a Postdoctoral Fellow in August 2011 and then as Biologist in February 2015. She became a full-time NIH Staff Scientist in 2020. Her current work is focused on dysregulated signaling pathways in pulmonary arterial hypertension (PAH), and the development of targeted therapies aimed at blocking the proliferative, hyper-migratory, anti-apoptotic pulmonary vascular phenotype associated with PAH. Bone morphogenetic protein type II receptor (BMPR2) loss-of-function is the most common molecular defect underlying heritable PAH. In human pulmonary artery endothelial cells (PAECs), BMPR2 silencing led to constitutive ERK and AKT activation, a disrupted cytoskeletal architecture and a proliferative/apoptosis-resistant phenotype recapitulating cellular abnormalities observed in late-stage PAH-endothelium.
