Steve Cannon MD, PhD
Steve Cannon is Professor of Neurology and Associate Dean for Medical Education at UT Southwestern Medical Center in Dallas, Texas. He received a BS and MS in mechanical engineering from Washington University in St Louis, and then completed MD training at Johns Hopkins Medical School. He also received a PhD in Biomedical Engineering from Johns Hopkins.
Dr. Cannon was a neurology resident at Massachusetts General Hospital and was then on the faculty at Harvard Medical School for 12 years. In 2002, he relocated to Dallas Texas to become the Chairman of Neurology at UT Southwestern Medical Center.
Dr. Cannon’s interest in periodic paralysis and myotonia began as a post-doctoral research fellow at Harvard Medical School in 1990. His laboratory has focused on the question of how ion channel function is altered by mutations associated with periodic paralysis or myotonia, and on why these defects in channel function predispose patients to attacks of muscle stiffness or weakness.
Important discoveries from his laboratory include:
* Sodium channel mutations associated with hyperkalemic periodic paralysis cause a gain-of-function defect by disruption of inactivation.
* Slow inactivation defects of sodium channels predispose to attacks of paralysis
* First comprehensive mathematical model for myotonia and periodic paralysis, both being consequences of impaired sodium channel inactivation
* Hypokalemic periodic paralysis mutations cause “leaky” sodium channels due to defects in the voltage-sensor mechanism
* Developed the first sodium channel knock-in mutant mouse model of hyperkalemic periodic paralysis (Dr. Lawrence Hayward, collaborator)
* Developed the first sodium channel knock-in mouse mutant model of hypokalemic periodic paralysis.
* Developed the first calcium channel knock-in mutant mouse model of hypokalemic periodic paralysis
* Research in the Cannon Laboratory has been generously supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the NIH, the Muscular Dystrophy Association, and the Howard Hughes Medical Institute.
Dr. Cannon received the Derek Denny-Brown Neurological Scholar Award from the American Neurological Association and a MERIT (Method of Extending Research in Time) Award from the NIH. He is a member of the Scientific Advisory Committee of the MDA and the Scientific Committee for the Telethon (Italy). Dr. Cannon is on the Editorial Boards of the Journal of General Physiology and the Journal of Neurotherapeutics.
Recent Publications:
* Cannon, S.C. 2006. Pathomechanisms in Channelopathies of Skeletal Muscle and Brain. Ann. Rev Neurosci. 2006, 29:387-415.
* Struyk, A.F. and Cannon, S.C. A Na+ channel mutation linked to hypokalemic periodic paralysis exposes a proton-selective gating pore. J. Gen. Physiol. 2007, 130: 11-20.
* Struyk A.F. and Cannon, S.C. Dissecting the physiology of aberrant depolarization in hypokalemic paralysis Muscle & Nerve. 2008, 37: 327-337.
* Hayward, L.J. Kim, J.S., Lee, M.Y., Zhou, H., Jang, G., Misra, K., Salajegheh, M., Wu F., Asada, C., Reid, V., Cros, D., Hoffman, E., Cannon, S.C., and Brown, Jr, R.H. Targeted Mutation of Mouse NaV1.4 Muscle
* Sodium Channel Reproduces Features of Hyperkalemic Periodic Paralysis. Journal of Clinical Investigation. 2008, 118: 1437-1449.
* Cannon, S. C. Voltage-sensor mutations in channelopathies of skeletal muscle. J Physiol. 2010, 588: 1887-1895.
* Francis, D., Rybalchenko, V., Struyk, A.F., Cannon, S.C. Sodium channel voltage sensor mutations in periodic paralysis, but not paramyotonia, produce a gating pore leak. Neurology 2011, 76:1635-1641.
