Keith Elmslie

Rapid and reversible block of N-type calcium channels (CaV 2.2) by omega-conotoxin GVIA in the absence of divalent cations.

Calcium channel blockers in the treatment of disease.

Neurotransmitter modulation of neuronal calcium channels.

Slowed N-type calcium channel (CaV2.2) deactivation by the cyclin-dependent kinase inhibitor roscovitine.

Ca2+ enhances U-type inactivation of N-type (CaV2.2) calcium current in rat sympathetic neurons.

Roscovitine differentially affects CaV2 and Kv channels by binding to the open state.

The separation of antagonist from agonist effects of trisubstituted purines on CaV2.2 (N-type) channels.

omega-conotoxin GVIA alters gating charge movement of N-type (CaV2.2) calcium channels.

The Timothy syndrome mutation of cardiac CaV1.2 (L-type) channels: multiple altered gating mechanisms and pharmacological restoration of inactivation.

State-dependent block of HERG potassium channels by R-roscovitine: implications for cancer therapy.

Open-state occupancy prevents gating charge relaxation of N-type (CaV2.2) calcium channels.

Roscovitine binds to novel L-channel (CaV1.2) sites that separately affect activation and inactivation.

A single amino acid change in Ca(v)1.2 channels eliminates the permeation and gating differences between Ca(2+) and Ba(2+).

Site-specific effects of diselenide bridges on the oxidative folding of a cystine knot peptide, omega-selenoconotoxin GVIA.

Phospholemman modulates the gating of cardiac L-type calcium channels.

Ceramide modulates HERG potassium channel gating by translocation into lipid rafts.

Interference between two modulators of N-type (CaV2.2) calcium channel gating demonstrates that omega-conotoxin GVIA disrupts open state gating.

The intravenous anesthetic propofol inhibits human L-type calcium channels by enhancing voltage-dependent inactivation.

Amino acid substitutions in the FXYD motif enhance phospholemman-induced modulation of cardiac L-type calcium channels.

Roscovitine inhibits CaV3.1 (T-type) channels by preferentially affecting closed-state inactivation.

Domain III regulates N-type (CaV2.2) calcium channel closing kinetics.

Dissecting a role of evolutionary-conserved but noncritical disulfide bridges in cysteine-rich peptides using ω-conotoxin GVIA and its selenocysteine analogs.

Tetrodotoxin-resistant voltage-dependent sodium channels in identified muscle afferent neurons.

NaV1.8 channels are expressed in large, as well as small, diameter sensory afferent neurons.

Identification of CaV channel types expressed in muscle afferent neurons.