Kathrin Banach
Assistant Professor
Department of Internal Medicine
Rush University
United States of America
Biography
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 Interest
Research area includes Cellular mechanisms of atrial fibrillation, p21-activated kinase.
Publications
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The C-terminus of the long AKAP13 isoform (AKAP-Lbc) is critical for development of compensatory cardiac hypertrophy. Taglieri DM, Johnson KR, Burmeister BT, Monasky MM, Spindler MJ, DeSantiago J, Banach K, Conklin BR, Carnegie GK. J Mol Cell Cardiol. 2014 Jan;66:27-40. doi: 10.1016/j.yjmcc.2013.10.010.
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p21-Activated kinase1 (Pak1) is a negative regulator of NADPH-oxidase 2 in ventricular myocytes. DeSantiago J, Bare DJ, Xiao L, Ke Y, Solaro RJ, Banach K. J Mol Cell Cardiol. 2014 Feb;67:77-85. doi: 10.1016/j.yjmcc.2013.12.017.
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Spatially defined InsP3-mediated signaling in embryonic stem cell-derived cardiomyocytes. Kapoor N, Maxwell JT, Mignery GA, Will D, Blatter LA, Banach K. PLoS One. 2014 Jan 7;9(1):e83715. doi: 10.1371/journal.pone.0083715. eCollection 2014.
