Professor and Chair of Physiology, David Geffen School of Medicine at UCLA
Neurology
Dr. Stephen C. Cannon, MD
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Stephen Cannon is an expert in the field of Neurology. He researched medicine at Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is one of the top medical schools in the US. Johns Hopkins University School of Medicine is ranked 3/29 in Research/PrimaryCare. He has 1 awards "Super Doctor". Stephen Cannon is a published physician as well. He has 67 publications published. The latest was: Enhanced slow inactivation by V445M: a sodium channel mutation associated with myotonia. He is registered with Medicare.
Publications
- Disrupted coupling of gating charge displacement to Na+ current activation for DIIS4 mutations in hypokalemic periodic paralysis.
- New territory opened by periodic paralysis associated with mitochondrial DNA mutation.
- Skeletal muscle-specific T-tubule protein STAC3 mediates voltage-induced Ca2+ release and contractility.
- Non-dystrophic myotonia: prospective study of objective and patient reported outcomes.
- Bumetanide prevents Transient decreases in muscle force in murine hypokalemic periodic paralysis.
- A sodium channel defect in hyperkalemic periodic paralysis: potassium-induced failure of inactivation.
- Defective slow inactivation of sodium channels contributes to familial periodic paralysis.
- Mexiletine block of Disease-associated mutations in S6 segments of the human skeletal muscle Na(+) channel.
- The human skeletal muscle Na channel mutation R669H associated with hypokalemic periodic paralysis enhances slow inactivation.
- Sodium channel defects in myotonia and periodic paralysis.
- Slow inactivation differs among mutant Na channels associated with myotonia and periodic paralysis.
- Slow inactivation does not affect movement of the fast inactivation gate in voltage-gated Na+ channels.
- Enhanced slow inactivation by V445M: a sodium channel mutation associated with myotonia.
- A new mutation in a family with cold-aggravated myotonia disrupts Na(+) channel inactivation.
- Sodium channel inactivation is impaired in equine hyperkalemic periodic paralysis.
- The position of the fast-inactivation gate during lidocaine block of voltage-gated Na+ channels.
- From mutation to myotonia in sodium channel Disorders.
- COOH-terminal truncated alpha(1S) subunits conduct current better than full-length dihydropyridine receptors.
- Gating of the L-type Ca channel in human skeletal myotubes: an activation defect caused by the hypokalemic periodic paralysis mutation R528H.
- A proposed mutation, Val781Ile, associated with hyperkalemic periodic paralysis and cardiac dysrhythmia is a benign polymorphism.
- Theoretical reconstruction of myotonia and paralysis caused by incomplete inactivation of sodium channels.
- Modulation of Na+ channel inactivation by the beta 1 subunit: a deletion analysis.
- Human sodium channel gating defects caused by missense mutations in S6 segments associated with myotonia: S804F and V1293I.
- Functional expression of sodium channel mutations identified in families with periodic paralysis.
- Modification of the Na+ current conducted by the rat skeletal muscle alpha subunit by coexpression with a human Brain beta subunit.
- Loss of Na+ channel inactivation by anemone toxin (ATX II) mimics the myotonic state in hyperkalaemic periodic paralysis.
- Effects of mutations causing hypokalaemic periodic paralysis on the skeletal muscle L-type Ca2+ channel expressed in Xenopus laevis oocytes.
- Rapid and slow voltage-dependent conformational changes in segment IVS6 of voltage-gated Na(+) channels.
- Spectrum of sodium channel disturbances in the nondystrophic myotonias and periodic paralyses.
- Ion-channel defects and aberrant excitability in myotonia and periodic paralysis.
- Slow inactivation of sodium channels: more than just a laboratory curiosity.
- The cloning and expression of a sodium channel beta 1-subunit cDNA from human Brain.
- Sequence of the voltage-gated sodium channel beta1-subunit in wild-type and in quivering mice.
- Chimeric mutations in the M2 segment of the 5-hydroxytryptamine-gated chloride channel MOD-1 define a minimal determinant of anion/cation permeability.
- Leukocyte common antigen-related phosphatase is a functional receptor for chondroitin sulfate proteoglycan axon growth inhibitors.
- The primary periodic paralyses: diagnosis, pathogenesis and treatment.
- MOD-1 is a serotonin-gated chloride channel that modulates locomotory behaviour in C. elegans.
- GAP-43 augments G protein-coupled receptor transduction in Xenopus laevis oocytes.
- Bilateral third Nerve palsy and temporal arteritis.
- Suppression subtractive hybridization identifies high glucose levels as a stimulus for expression of connective tissue growth factor and other genes in human mesangial...
- The non-dystrophic myotonias: molecular pathogenesis, diagnosis and treatment.
- Sodium channel gating: no margin for error.
- An expanding view for the molecular basis of familial periodic paralysis.
- Expanded CUG repeats trigger aberrant splicing of ClC-1 chloride channel pre-mRNA and hyperexcitability of skeletal muscle in myotonic dystrophy.
- Slow inactivation does not block the aqueous accessibility to the outer pore of voltage-gated Na channels.
- Myasthenic syndrome caused by mutation of the SCN4A sodium channel.
- Paying the price at the pump: dystonia from mutations in a Na+/K+ -ATPase.
- Truncated ClC-1 mRNA in myotonic dystrophy exerts a dominant-negative effect on the Cl current.
- A C-terminal skeletal muscle sodium channel mutation associated with myotonia disrupts fast inactivation.
- Pathomechanisms in channelopathies of skeletal muscle and Brain.
- Physiologic principles underlying ion channelopathies.
- A Na+ channel mutation linked to hypokalemic periodic paralysis exposes a proton-selective gating pore.
- Cold-induced defects of sodium channel gating in atypical periodic paralysis plus myotonia.
- Paradoxical depolarization of BA2+- treated muscle exposed to low extracellular K+: insights into resting potential abnormalities in hypokalemic paralysis.
- Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium-sensitive weakness.
- Gating pore currents in DIIS4 mutations of NaV1.4 associated with periodic paralysis: saturation of ion flux and implications for Disease pathogenesis.
- Slow inactivation of the NaV1.4 sodium channel in mammalian cells is impeded by co-expression of the beta1 subunit.
- Getting a charge out of periodic paralysis?
- Sodium channels gone wild: resurgent current from neuronal and muscle channelopathies.
- Voltage-sensor mutations in channelopathies of skeletal muscle.
- Leaky sodium channels from voltage sensor mutations in periodic paralysis, but not paramyotonia.
- Identification and functional characterization of Kir2.6 mutations associated with non-familial hypokalemic periodic paralysis.
- The common missense mutation D489N in TRIM32 causing limb girdle muscular dystrophy 2H leads to loss of the mutated protein in knock-in mice resulting in a Trim32-null...
- A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis.
- Gating behaviour of sodium currents in adult mouse muscle recorded with an improved two-electrode voltage clamp.
- Inactivation defects caused by myotonia-associated mutations in the sodium channel III-IV linker.
Schools
Johns Hopkins University School of Medicine
Mass Genl
Procedures Preformed
- EEG (Electroencephalogram)
- EMG (Electromyography)
Conditions Treated
- Alzheimer's Disease
- Ataxia
- Brain Aneurysm
- Cerebrovascular Disease
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Doctors Specialties
- Neurology
Accepted Insurances
- Choice Plus POS II
- Power Select HMO
- Blue Card PPO
- CaliforniaCare HMO
- Advantage Preferred DirectAccess Plus PPO
- Blue Cross Blue Shield of California PPO
- Select Plus HMO
- Select PPO
- Blue Choice
- Access Plus Savenet
- Basic PPO
- Enhanced Exclusive for Small Business HMO
- Local Access Plus HMO
- Cigna HMO
- Great West Healthcare-Cigna PPO
- LocalPlus
- Commercial Insurance Company
- First Health (Coventry Health Care) PPO
- Choice Care PPO
- Preferred PPO
- Medicaid
- Medicare MCR
- Molina
- MultiPlan PPO
- PHCS Network PPO
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- Universal American
Awards
- Super Doctor
Education
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Massachusetts General Hospital -
Johns Hopkins University School of Medicine
Hospital
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University of Texas Southwestern Medical Center
Drug Facts
| NPI NUMBER | 1962461095 | |
| NPPES Provider LastName | CANNON | |
| NPPES Provider FirstName | STEPHEN | |
| NPPES Provider ZIPCode | 753907208 | |
| NPPES Provider State | TX | |
| Specialty Description | Neurology | |
| Total Claim Count | 44.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1962461095 |
| Last Name Of The Provider | CANNON |
| First Name Of The Provider | STEPHEN |
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