Dr. Martina Gentzsch is an Associate Professor of Cell Biology and Physiology at the University of North Carolina at Chapel Hill. A major goal of Dr. Gentzsch's studies is to uncover potential targets that are of clinical interest for cystic fibrosis (CF) therapy and permit pharmacological modulation of CFTR in physiologically relevant CF model systems. She received her Ph.D. from the University of Regensburg, Germany in 1997 and has been working in the field of CFTR research for more than 15 years. Dr. Gentzsch is a well-recognized expert in biochemistry and cell biology of ion channel trafficking. As a postdoctoral fellow at the Mayo Clinic in the laboratory of Dr. John R. Riordan, who co-discovered the CFTR gene, she carried out crucial studies on CFTR processing and its intracellular trafficking. As Assistant Professor of Cell and Cell Biology and Physiology at the at the University of North Carolina at Chapel Hill, she established novel techniques to evaluate rescue of CFTR by small-molecule compounds and developed reliable methodology to track apical stability of mutant CFTR in physiologically relevant well-differentiated primary human bronchial epithelial (HBE) and human nasal epithelial (HNE) cultures. In 2012, Dr. Gentzsch assumed the role of Director of the CFTR Correction Core that was specialized to perform electrophysiological measurements to determine the extent of mutant CFTR rescue in primary epithelial cultures and tissues. Using the capabilities of the Core, her research revealed that FDA-approved CFTR potentiator VX-770 drastically impedes correction of F508del CFTR by increasing turnover of the rescued protein. More recently, as an Associate Professor at UNC, she developed state-of-the-art pre-clinical assays to investigate the efficacy of novel therapeutic approaches to CF in relevant models of CF including intestinal, nasal, and bronchial organoids. Since 2015, she directs the CF RTCC Pre-Clinical Core that supports the translation of therapeutic strategies for CF from basic research to clinical studies. This Core provides assessment of drug candidates in physiologically relevant in vitro, ex vivo, and in vivo models. Furthermore, she has established the RDP CFTR Functional Analysis Core that is specialized in characterizing expression, rescue, and activity of CFTR in HBE and HNE cells from CF patients. Currently Dr. Gentzsch is investigating 1) means to rescue rare CFTR mutations, 2) mechanistic details on how environmental factors such as inflammation affect CFTR rescue, 3) tissue-specific rescue of CFTR, 4) consequences of CFTR rescue for mucociliary clearance in CF airways, and 5) the impact of genetic modifiers of CF on CFTR function and rescue.