Lane L Clarke D.V.M.,Ph.D.

University of Missouri

Lane L. Clarke, D.V.M., Ph.D. is a Professor of Biomedical Sciences, College of Veterinary Medicine and Dalton Cardiovascular Research Center at the University of Missouri. Dr. Clarke received a D.V.M. and a M.S. in Physiology from the University of Missouri College of Veterinary Medicine in 1982. Following several years of clinical practice, Dr. Clarke matriculated at North Carolina State University where he received a Ph.D. in gastrointestinal physiology in 1989 (R.A. Argenzio, mentor). In post-doctoral studies at the University of North Carolina Cystic Fibrosis Research Center (R.C. Boucher, mentor), Dr. Clarke participated in the original studies of airway and intestinal dysfunction in the first cystic fibrosis mouse model. At the University of Missouri College of Veterinary Medicine, Dr. Clarke was appointed assistant professor in 1993 and rose through the ranks to full professor in 2007. He has served on the editorial board of the American Journal of Physiology, the NIH study section Clinical, Integrative and Molecular Gastroenterology and currently serves on the Research and Research Training Committee of the Cystic Fibrosis Foundation. Dr. Clarke's research investigates abnormalities of acid-base transporters in cystic fibrosis and other genetic diseases as they relate to intestinal stem cell biology (ISCs) and differentiation of secretory cells. Studies of mice with gene-targeted deletion of CFTR (a cAMP-regulated Cl- and HCO3- ion channel) or other acid-base transporters are performed in vivo or using regenerating murine intestinal organoids grown in 3D gel culture. Principal discovery techniques involve confocal microfluorimetry, electrophysiology and measures of gene expression. Current projects investigate a) the role of CFTR in down-regulating cell cycle dynamics and Wnt/beta-catenin signaling in ISCs; b) the role of CFTR in goblet cell mucus exocytosis in the intestine; and c) the expression and function of human CFTR in a newly-developed mouse model in which murine Cftr is replaced by the human ortholog of the gene, i.e., hCFTR rescue┬Ł mouse.