Stephen C. Cannon

Efficacy of a K<sup>+</sup> Channel Agonist, XEN1101, For Preserving Contractility in Mouse Models of Hypokalemic Periodic Paralysis.

The molecular transition that confers voltage dependence to muscle contraction.

Potassium-sensitive loss of muscle force in the setting of reduced inward rectifier K<sup>+</sup> current: Implications for Andersen-Tawil syndrome.

Periodic paralysis

Retigabine suppresses loss of force in mouse models of hypokalaemic periodic paralysis.

Voltage-dependent Ca<sup>2+</sup> release is impaired in hypokalemic periodic paralysis caused by Ca<sub>V</sub>1.1-R528H but not by Na<sub>V</sub>1.4-R669H.

Voltage-Dependent Ca ²⁺ Release Is Impaired in Hypokalemic Periodic Paralysis Caused by Ca _V 1.1-R528H but not by Na _V 1.4-R669H

Retigabine Suppresses Loss of Force in a Mouse Model of Hypokalemic Periodic Paralysis

The distinct role of the four voltage sensors of the skeletal CaV1.1 channel in voltage-dependent activation.

Gating pore currents occur in CaV1.1 domain III mutants associated with HypoPP.

Epilepsy channelopathies go neddy: stabilizing NaV1.1 channels by neddylation

Guidelines on clinical presentation and management of nondystrophic myotonias

Further evidence for shared genetic susceptibility in both sporadic and Thyrotoxic periodic paralysis

A role for external Ca2+ in maintaining muscle contractility in periodic paralysis

Resurgent and Gating Pore Currents Induced by <i>De Novo SCN2A</i> Epilepsy Mutations.

Myasthenic congenital myopathy from recessive mutations at a single residue in Na&lt;sub&gt;V&lt;/sub&gt;1.4.

A four-electrode method to study dynamics of ion activity and transport in skeletal muscle fibers.

Recovery from acidosis is a robust trigger for loss of force in murine hypokalemic periodic paralysis.

Review of the Diagnosis and Treatment of Periodic Paralysis

Sodium Channelopathies of Skeletal Muscle

Channelopathies of Skeletal Muscle Excitability