Roger A. Bannister

Reconstituted slow muscarinic inhibition of neuronal (Ca(v)1.2c) L-type Ca2+ channels.

Mapping sites of potential proximity between the dihydropyridine receptor and RyR1 in muscle using a cyan fluorescent protein-yellow fluorescent protein tandem as a fluorescence resonance energy transfer probe.

Neurokinin 1 receptors trigger overlapping stimulation and inhibition of CaV2.3 (R-type) calcium channels.

Bridging the myoplasmic gap: recent developments in skeletal muscle excitation-contraction coupling.

The alpha(1S) III-IV loop influences 1,4-dihydropyridine receptor gating but is not directly involved in excitation-contraction coupling interactions with the type 1 ryanodine receptor.

The monomeric G proteins AGS1 and Rhes selectively influence Galphai-dependent signaling to modulate N-type (CaV2.2) calcium channels.

The skeletal L-type Ca(2+) current is a major contributor to excitation-coupled Ca(2+) entry.

Reassessing the molecular mechanism of beta-adrenergic stimulation of cardiac L-type Ca2+ current.

Effects of inserting fluorescent proteins into the alpha1S II-III loop: insights into excitation-contraction coupling.

The cardiac alpha(1C) subunit can support excitation-triggered Ca2+ entry in dysgenic and dyspedic myotubes.

The 63rd Symposium of the Society of General Physiologists: "muscles" instead of squid at Woods Hole.

A malignant hyperthermia-inducing mutation in RYR1 (R163C): consequent alterations in the functional properties of DHPR channels.

A malignant hyperthermia-inducing mutation in RYR1 (R163C): alterations in Ca2+ entry, release, and retrograde signaling to the DHPR.

Looking for answers to EC coupling's persistent questions.

Properties of Na+ currents conducted by a skeletal muscle L-type Ca2+ channel pore mutant (SkEIIIK).

A shortcut to a skeletal muscle DHPR knock-in?

Malignant hyperthermia susceptibility arising from altered resting coupling between the skeletal muscle L-type Ca2+ channel and the type 1 ryanodine receptor.

Triclosan impairs excitation-contraction coupling and Ca2+ dynamics in striated muscle.

Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.

Impaired gating of an L-Type Ca(2+) channel carrying a mutation linked to malignant hyperthermia.

Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate.

RGK protein-mediated impairment of slow depolarization- dependent Ca2+ entry into developing myotubes.

Functional assessment of three Rem residues identified as critical for interactions with Ca(2+) channel β subunits.

Apparent lack of physical or functional interaction between CaV1.1 and its distal C terminus.

Rem uncouples excitation-contraction coupling in adult skeletal muscle fibers.

Bridging the myoplasmic gap II: more recent advances in skeletal muscle excitation-contraction coupling.

Distinct Components of Retrograde Ca(V)1.1-RyR1 Coupling Revealed by a Lethal Mutation in RyR1.

Defining the MO's of RGK proteins.

Progressive impairment of CaV1.1 function in the skeletal muscle of mice expressing a mutant type 1 Cu/Zn superoxide dismutase (G93A) linked to amyotrophic lateral sclerosis.