Competitive modulation of K1.2 gating by LMAN2 and Slc7a5.

K1.2 is a prominent ion channel in the CNS, where it regulates neuronal excitability. K1.

Regulation of Kv1.2 Redox-Sensitive Gating by the Transmembrane Lectin LMAN2.

Voltage gated potassium (Kv)1.2 channels influence excitability and action potential propagation in the nervous system. Unlike closely related Kv1 channels, Kv1.

Symptom Burden and Time from Symptom Onset to Cancer Diagnosis in Patients with Early-Onset Colorectal Cancer: A Multicenter Retrospective Analysis.

: The incidence of colorectal cancer (CRC) is decreasing in individuals >50 years due to organised screening but has increased for younger individuals. We characterized symptoms and their timing before diagnosis in young individuals. : We identified all patients diagnosed with CRC between 1990-2017 in British Columbia, Canada.

Unmasking subtype-dependent susceptibility to C-type inactivation in mammalian Kv1 channels.

Shaker potassium channels have been an essential model for studying inactivation of ion channels and shaped our earliest understanding of N-type vs. C-type mechanisms. In early work describing C-type inactivation, López-Barneo and colleagues systematically characterized numerous mutations of Shaker residue T449, demonstrating that this position was a key determinant of C-type inactivation rate.

Control of Slc7a5 sensitivity by the voltage-sensing domain of Kv1 channels.

Many voltage-dependent ion channels are regulated by accessory proteins. We recently reported powerful regulation of Kv1.2 potassium channels by the amino acid transporter Slc7a5.

Slc7a5 regulates Kv1.2 channels and modifies functional outcomes of epilepsy-linked channel mutations.

Kv1.2 is a prominent voltage-gated potassium channel that influences action potential generation and propagation in the central nervous system. We explored multi-protein complexes containing Kv1.

Extracellular redox sensitivity of Kv1.2 potassium channels.

Kv1.2 is a prominent potassium channel subtype in the nervous system and serves as an important structural template for investigation of ion channel function. However, Kv1.

Determinants of frequency-dependent regulation of Kv1.2-containing potassium channels.

Voltage-gated potassium channels are important regulators of electrical excitation in many tissues, with Kv1.2 standing out as an essential contributor in the CNS. Genetic deletion of Kv1.

Use-dependent activation of neuronal Kv1.2 channel complexes.

In excitable cells, ion channels are frequently challenged by repetitive stimuli, and their responses shape cellular behavior by regulating the duration and termination of bursts of action potentials. We have investigated the behavior of Shaker family voltage-gated potassium (Kv) channels subjected to repetitive stimuli, with a particular focus on Kv1.2.

Inward rectifiers and their regulation by endogenous polyamines.

Inwardly-rectifying potassium (Kir) channels contribute to maintenance of the resting membrane potential and regulation of electrical excitation in many cell types. Strongly rectifying Kir channels exhibit a very steep voltage dependence resulting in silencing of their activity at depolarized membrane voltages. The mechanism underlying this steep voltage dependence is blockade by endogenous polyamines.