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).
|Medical School||Johns Hopkins Hospital (1986)|
|Internship||Massachusetts General Hospital (1987), Internal Medicine|
|Residency||Massachusetts General Hospital (1990), Neurology|
|Fellowship||Massachusetts General Hospital (1994), Neurobiology|
- Ion channel physiology
- mathematical modeling
- mouse model of muscle disease
- periodic paralysis
- skeletal muscle
- Bumetanide prevents transient decreases in muscle force in murine hypokalemic periodic paralysis.
- Wu F, Mi W, Cannon SC Neurology 2013 Feb
- A calcium channel mutant mouse model of hypokalemic periodic paralysis.
- Wu F, Mi W, Hernández-Ochoa EO, Burns DK, Fu Y, Gray HF, Struyk AF, Schneider MF, Cannon SC J. Clin. Invest. 2012 Dec 122 12 4580-91
- A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis.
- Wu F, Mi W, Burns DK, Fu Y, Gray HF, Struyk AF, Cannon SC J. Clin. Invest. 2011 Oct 121 10 4082-94
- Gating pore currents in DIIS4 mutations of NaV1.4 associated with periodic paralysis: saturation of ion flux and implications for disease pathogenesis.
- Struyk AF, Markin VS, Francis D, Cannon SC J. Gen. Physiol. 2008 Oct 132 4 447-64
- Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium-sensitive weakness.
- Hayward LJ, Kim JS, Lee MY, Zhou H, Kim JW, Misra K, Salajegheh M, Wu FF, Matsuda C, Reid V, Cros D, Hoffman EP, Renaud JM, Cannon SC, Brown RH J. Clin. Invest. 2008 Apr 118 4 1437-49
- 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
- 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
- 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
- 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
- Beneficial effects of bumetanide in a CaV1.1-R528H mouse model of hypokalaemic periodic paralysis.
- Wu F, Mi W, Cannon SC Brain 2013 Oct
Honors & Awards
- Patricia A. Smith Distinguished Chair in Neuromuscular Research
- MERIT Award - NIH
- Derek Denny-Brown Neurological Scholar Award