David C. Dawson, PhD

DCD Hood- June 2005

Primary Affiliation

Professor Emeritus

Program Affiliation

Physiology & Pharmacology
Neuroscience Graduate Program
Program in Molecular & Cellular Biosciences

Background & Education

B.S. Electrical Engineering ,University of Pittsburgh, 1966

Ph.D. Physiology, University of Pittsburgh, 1971

Postdoctoral, Yale University, 1971-73

Assistant/Associate Professor Physiology & Biophysics, University of Iowa 1973-1980

Associate Professor/Professor Physiology, University of Michigan 1980-1999


Structure and function of the CFTR Chloride Channel.

Searching for the cure for two lethal childhood diseases: Most people are surprised to learn that two devastating childhood diseases, cystic fibrosis and secretory diarrhea are closely linked. Cystic Fibrosis is the most common lethal genetic disease among Caucasians, affecting 1/2500 live births. Although the cystic fibrosis gene was identified nearly 20 years ago, a cure for the disease has remained elusive. Secretory diarrhea is an infectious disease that is the leading cause of infant death world-wide. A major world health problem, diarrheal disease causes billions of dollars of lost productivity in the U.S. alone. Both of these diseases are caused by abnormal regulation of the same molecule, a protein called CFTR that is found in cells of the human lung, pancreas, liver and GI tract. The protein functions as a gate (a chloride channel) which controls the movement of chloride ions out of cells.

The goal of the research carried out in Dr. Dawson's lab is to provide the scientific basis for the development of drugs that can be used to treat these two lethal diseases of childhood. The research combines high-resolution electrophysiological measurements of CFTR's channel properties with chemical modification strategies designed to reveal what parts of the CFTR molecule are most important for its vital functions. This information is used to refine atomic-scale models for the protien. Understanding how this complex molecule does its job will provide the foundation for the design drugs or other therapies that can be used to increase the activity of CFTR in cystic fibrosis patients or to decrease the activity of CFTR in people suffering from secretory diarrhea.



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