All rapid physiological processes are triggered by electrical signals. Voltage-gated sodium channels initiate action potentials and voltage-gated calcium channels initiate contraction, secretion, neurotransmission, and more. Dysfunction of these channels causes epilepsy, cardiac arrhythmia, and chronic pain. Recent discovery of bacterial ancestors of sodium and calcium channels has allowed us to determine the structural basis for voltage-dependent activation, inactivation, and rapid, highly selective ion conductance at atomic resolution. These channels are targets for drugs used for pain, epilepsy, arrhythmia, hypertension, and angina. The binding sites for these drugs are now being elucidated at atomic resolution, with important implications for structure-based drug design.
Bill Catterall received a B.A. in Chemistry from Brown University in 1968, a Ph.D. in Physiological Chemistry from Johns Hopkins in 1972, and postdoctoral training in neurobiology and molecular pharmacology as a Muscular Dystrophy Association Fellow with Dr. Marshall Nirenberg at the National Institutes of Health from 1972 to 1974. Following three years as a staff scientist at NIH, he joined the University of Washington in 1977 as Associate Professor of Pharmacology, became Professor in 1981, and Chair from 1984 to 2016. Catterall discovered the voltage-gated sodium and calcium channel proteins, which initiate electrical and chemical signaling in excitable cells, and his work has contributed much to understanding their structure, function, regulation, and molecular pharmacology. Catterall is a member of several science academies, including the US National Academy of Science, the Institute of Medicine, and the Royal Society of London, UK. He has received numerous awards, including the Gairdner International Award of Canada in 2010.
The Peter Garland Lecture was set up in 1985 to mark the achievement of Dundee’s first Professor of Biochemistry in building up the Department into one of the strongest in the UK over the period 1970 to 1984.