Assistant Professor
Department of Internal Medicine
Rush University
United States of America
Banach’s research focuses on the cellular mechanism of atrial fibrillation (AF), the most common cardiac arrhythmia in clinical practice that can precipitate heart failure, stroke and even death. In an ongoing project, her team determined that the expression of the p21-activated kinase (Pak1) is decreased in the etiology of AF in patients and animal models of AF, and that attenuation of atrial Pak1 activity increases atrial arrhythmic activity. The current aims of her laboratory are to determine the molecular mechanisms involved in the following processes: How Pak1 is reduced in patients with AF How reduced Pak1 increases the propensity of AF due to increased trigger activity and tissue remodeling How Pak1 is a negative regulator of cellular production of reactive oxygen species How stabilization of Pak1 expression can attenuate AF
Research area includes Cellular mechanisms of atrial fibrillation, p21-activated kinase.