Stephen Cannon, MD, PhD

Associate Dean for Undergraduate Medical Education, Basic Sciences
Professor
Neurology and Neurotherapeutics
Graduate Program: Integrative Biology
Neuroscience

Contact Information

UT Southwestern Medical Center
5323 Harry Hines Boulevard
Dallas, Texas 75390

steve.cannon@utsouthwestern.edu

To make an appointment, call 214-645-8300.

Biography

The primary research interests of our laboratory are how ion channels regulate the electrical excitability of cells and how defects in these channels lead to human disease. Electrical signaling is a fundamental mechanism by which cells initiate and regulate contraction of muscles, beating of the heart, secretion of hormones, and communication among neurons. Ion channels are crucial components of the machinery to accomplish this signaling, by forming pores in the cell membrane to allow the passage of electric current. In the past decade, mutations of ion channel genes have been found for inherited diseases that cause episodic paralysis, familial migraine, episodic ataxia, fatal cardiac arrhythmias, and some forms of epilepsy. We have been studying the consequences of mutations in sodium and calcium channels that have been linked to muscle disorders causing episodic paralysis or stiffness (myotonia).

Education

FellowshipMassachusetts General Hospital, Neurology (1994)
ResidencyMassachusetts General Hospital, Neurology (1990)
InternshipMassachusetts General Hospital, Internal Medicine (1987)
Medical SchoolJohns Hopkins Hospital (1986)

Research Interests

electrophysiology
Ion channel physiology
myotonia
periodic paralysis

Publications

Featured
A Na+ Channel Mutation Linked to Hypokalemic Periodic Paralysis Exposes a Proton-selective Gating Pore

Struyk, A. and Cannon, S.C. , Journal of General Physiology , July 2007; (130):11-20

Featured
Accumulation of poly(CUG) or (CCUG) RNA in the nucleus triggers aberrant splicing of chloride channel 1 pre-mRNA and chloride channelopathy in myotonic dystrophy

Mankodi, A., Takahashi, M.P., Jiang H., Beck, C., Bowers, W., Moxley, R.T., Cannon, S.C., Thornton, C. , Molecular Cell , 2002; (10):35-44

Featured
MOD-1 is a serotonin-gated chloride channel that modulates C. elegans locomotory behaviour.

Ranganathan R., Cannon, SC, Horvitz, RH , Nature , 2000; (408):470-475

Featured
A sodium channel defect in hyperkalemic periodic paralysis: potassium-induced failure of inactivation

Cannon, S.C., Brown, R.H., Corey, D.P. , Neuron , 1991; (6):619-626

Myasthenic syndrome caused by mutation of the SCN4A sodium channel

Tsujino, A., Maertens, C., Ohno, K., Shen, X. M., Fukuda, T., Harper, C. M, Cannon, S. C., Engel, A. G. , Proc Natl Acad Sci U S A , June 2003; (100 (12)):7377-7382

A Na+ Channel Mutation Linked to Hypokalemic Periodic Paralysis Exposes a Proton-selective Gating Pore

Struyk, A. and Cannon, S.C. , Journal of General Physiology , July 2007; (130):11-20

Slow inactivation does not affect the aqueous accessibility of outer pore-lining residues of voltage-gated Na channels

Struyk, A.S. and Cannon, S.C , Journal of General Physiology , 2002; (120):509-516

The human skeletal muscle Na channel mutation R669H associated with hypokalemic periodic paralysis enhances slow inactivation

Struyk, A.S. and Cannon, S.C. , J. Neurosci , 2000; (20):8610-8617

Honors/Awards

Derek Denny-Brown Neurological Scholar Award

(2000)