Jason Scragg

Analysis of oxygen-sensitive human cardiac L-type Ca2+ channel alpha1C subunit (hHT Isoform).

Testosterone is a potent inhibitor of L-type Ca(2+) channels.

Alzheimer's amyloid peptides mediate hypoxic up-regulation of L-type Ca2+ channels.

Constitutive activity of endogenous receptors by inducible Gq overexpression.

Constitutive activity of human angiotensin II type-1 receptors by Gq overexpression.

A central role for ROS in the functional remodelling of L-type Ca2+ channels by hypoxia.

Molecular requirements for L-type Ca2+ channel blockade by testosterone.

H2O 2-stimulated Ca2+ influx via TRPM2 is not the sole determinant of subsequent cell death.

Modulation of hTREK-1 by carbon monoxide.

Carbon monoxide inhibits L-type Ca2+ channels via redox modulation of key cysteine residues by mitochondrial reactive oxygen species.

Ion channels as effectors in carbon monoxide signaling.

Hypoxia and neurodegeneration.

Carbon monoxide protects against oxidant-induced apoptosis via inhibition of Kv2.1.

Modulation of ion channels by hydrogen sulfide.

Cellular consequences of the expression of Alzheimer's disease-causing presenilin 1 mutations in human neuroblastoma (SH-SY5Y) cells.

Carbon monoxide mediates the anti-apoptotic effects of heme oxygenase-1 in medulloblastoma DAOY cells via K+ channel inhibition.

Carbon monoxide induces cardiac arrhythmia via induction of the late Na+ current.

Carbon monoxide inhibition of Cav3.2 T-type Ca2+ channels reveals tonic modulation by thioredoxin.

Inhibition of the cardiac Na⁺ channel Nav1.5 by carbon monoxide.

Heme oxygenase-1 regulates cell proliferation via carbon monoxide-mediated inhibition of T-type Ca2+ channels.

Hydrogen sulfide inhibits Cav3.2 T-type Ca2+ channels.

Oxygen-dependent hydroxylation by FIH regulates the TRPV3 ion channel.

H2S does not regulate proliferation via T-type Ca2+ channels.

Heme Oxygenase-1 Influences Apoptosis via CO-mediated Inhibition of K+ Channels.

Inhibition of T-type Ca2+ Channels by Hydrogen Sulfide.

Regulation of the T-type Ca(2+) channel Cav3.2 by hydrogen sulfide: emerging controversies concerning the role of H2 S in nociception.

Redox-Dependent Modulation of T-Type Ca(2+) Channels in Sensory Neurons Contributes to Acute Anti-Nociceptive Effect of Substance P.

Heme oxygenase-1 derived carbon monoxide suppresses Aβ toxicity in astrocytes.

A key role for peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) K channels in carbon monoxide-induced proarrhythmic early afterdepolarizations.

Multiple mechanisms mediating carbon monoxide inhibition of the voltage-gated K channel Kv1.5.

Piezo1 channel activation mimics high glucose as a stimulator of insulin release.

Unique Transcriptome Signature Distinguishes Patients With Heart Failure With Myopathy.

Brown and beige adipose tissue regulate systemic metabolism through a metabolite interorgan signaling axis.

Kv1.3 voltage-gated potassium channels link cellular respiration to proliferation through a non-conducting mechanism.

Hydrogen sulfide regulates hippocampal neuron excitability via S-sulfhydration of Kv2.1.

Inhibition of the voltage-gated potassium channel Kv1.5 by hydrogen sulfide attenuates remodeling through S-nitrosylation-mediated signaling.