SCN3B

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel beta subunit gene family, and influences the inactivation kinetics of the sodium channel. Two alternatively spliced variants, encoding the same protein, have been identified.

Sodium Voltage-Gated Channel Beta Subunit 3

Modulates channel gating kinetics. Causes unique persistent sodium currents. Inactivates the sodium channel opening more slowly than the subunit beta-1. Its association with NFASC may target the sodium channels to the nodes of Ranvier of developing axons and retain these channels at the nodes in mature myelinated axons (By similarity).

Biological Process atrial cardiac muscle cell action potentialManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process cardiac muscle cell action potential involved in contractionManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process cardiac muscle contractionManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process membrane depolarizationManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process membrane depolarization during action potentialManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process membrane depolarization during cardiac muscle cell action potentialManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process nervous system developmentIEA:Ensembl
Biological Process positive regulation of heart rateISS:BHF-UCL
Biological Process positive regulation of sodium ion transportManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process protein localization to plasma membraneManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process regulation of atrial cardiac muscle cell membrane depolarizationManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process regulation of heart rate by cardiac conductionManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process regulation of sodium ion transmembrane transporter activityManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process regulation of ventricular cardiac muscle cell membrane depolarizationManual Assertion Based On ExperimentIMP:BHF-UCL
Biological Process SA node cell action potentialISS:BHF-UCL
Biological Process sensory perception of painIEA:Ensembl
Biological Process sodium ion transmembrane transportManual Assertion Based On ExperimentIDA:BHF-UCL
Biological Process sodium ion transport1 PublicationNAS:UniProtKB
Biological Process ventricular cardiac muscle cell action potentialManual Assertion Based On ExperimentIMP:BHF-UCL

Membrane

Brugada syndrome 7 (BRGDA7):
A tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram (ECG). It can cause the ventricles to beat so fast that the blood is prevented from circulating efficiently in the body. When this situation occurs, the individual will faint and may die in a few minutes if the heart is not reset.
Atrial fibrillation, familial, 16 (ATFB16):
A familial form of atrial fibrillation, a common sustained cardiac rhythm disturbance. Atrial fibrillation is characterized by disorganized atrial electrical activity and ineffective atrial contraction promoting blood stasis in the atria and reduces ventricular filling. It can result in palpitations, syncope, thromboembolic stroke, and congestive heart failure.

Extracellular: 23-159
Helical: 160-180
Cytoplasmic: 181-215