Maintenance of the reactive oxygen species (ROS) homeostasis is essential to preserve cell integrity and is thus vital for the survival and growth of almost all life. Research in our lab aims to understand

• the architecture of mammalian ROS-generating enzymes, NADPH oxidases

• the activation and regulation mechanism underlying NADPH oxidases

• how to target NADPH oxidases for disease treatment

Parkinson's Disease (PD) is the second most common neurodegenerative disease. Genetic mutations in the LRRK2 gene are one of the leading causes for late onset PD cases. LRRK2 signaling plays a key role in the pathogenesis of both familial and sporadic PD cases. In our lab, we focus on two fundamental questions to understand the role of LRRK2 kinase in PD. 1) How do LRRK2 mutations lead to PD?  2) How can we target LRRK2 for PD treatment?

Ion channels conduct electron signals across the cell membrane and are essential for almost all physiological processes. KCNQ1 is the pore-forming subunit of IKs channel complexes and conducts the cardiac slow delayed rectifier current. Mutations in the kcnq1 gene are the leading cause of generic long-QT syndromes and cause sudden death to 3000-4000 young kids in US per year. We dissect the working mechanism of KCNQ1 and its modulation by different cellular signals. 

Cilia are slender, hair-like structures that extend from the surface of cells in many different organisms, including humans. These structures play a critical role in a variety of biological processes, including movement, sensory perception, and the maintenance of cellular and tissue structure. For example, in the respiratory system, cilia lining the airways help to move mucus and debris out of the lungs. We study the trafficking of key signaling molecules in and out of the cilia as well as their disease implications.