Phd Graduate Student
CurrentThe control of cellular redox balance is essential for upholding cardiovascular function and an imbalance of redox signaling is a central tenant contributing to the molecular underpinnings of cardiovascular disease. Therefore, understanding the translational impact of redox balance and signaling in the cardiovascular system (CV) is a focal point in our lab. Our lab has demonstrated that cytochrome b5 reductase 3 (CYB5R3) is a redox regulator by regulating the redox state of several critical substrates in cardiovascular cells, such as soluble guanylyl cyclase (sGC). The failure to reduce sGC results in loss of appropriate nitric oxide (NO) signaling, leading to a loss of vasodilation in the vasculature. Despite our extensive knowledge of CYB5R3 redox regulation in the CV system, nothing is known about the other CYB5R family members (CYB5R1, CYB5R2, CYB5R4, CYB5R5) in the CV system. My project aims to interrogate the redox regulatory roles of CYB5R1 in vascular endothelial cells. Techniques: cell culture, molecular cloning, protein purification, immunoblotting, electron paramagnetic resonance, mass spectrometry, flow cytometry, APEX biotinylation, co-IP, PCR, immunostaining, electron microscopy, fluorescence microscopy, myography, animal husbandry.