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The protein encoded by SCN4B is one of several sodium channel beta subunits. Additionally we are shipping Sodium Channel, Voltage-Gated, Type IV, beta Subunit Antibodies (21) and many more products for this protein.
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Data suggest that extracellular domains of Scn4b directly interact with each other in parallel homodimers that involve an intermolecular disulfide bond between unpaired Cys (show DNAJC5 Proteins) residues (Cys58) in loop connecting strands B and C and intermolecular hydrophobic and hydrogen-bonding interactions of N-terminal segments (Ser30-Val35); Scn4b homodimers appear to play role in cell-cell adhesion.
Scn4b(-/-) animals have deficits in motor coordination and balance and that firing rates in Scn4b(-/-) Purkinje neurons are markedly attenuated.
NaVbeta4 plays a blocking role that indicates the relative importance of different residues in inducing open-channel block.
Data show that Na(V)beta4 (Scn4b} expression determines multiple aspects of Na channel gating, thereby regulating excitability in cultured cerebellar granule cells.
down-regulation of Scn4b may lead to abnormalities of sodium channel and neurite degeneration in the striatum of Huntington's disease transgenic mice
Data suggest that extracellular domains of SCN4B directly interact with each other in parallel homodimers that involve an intermolecular disulfide bond between unpaired Cys (show DNAJC5 Proteins) residues (Cys58) in loop connecting strands B and C and intermolecular hydrophobic and hydrogen-bonding interactions of N-terminal segments (Ser30-Val35); SCN4B homodimers appear to play role in cell-cell adhesion.
The expression of a human-specific isoform of the voltage-gated sodium channel subunit SCN4B was significantly correlated to lifetime alcohol consumption
Contribution of Cardiac Sodium Channel (show SCN5A Proteins) beta-Subunit (show POLG Proteins) Variants to Brugada Syndrome.
Human Nav1.6 (show SCN8A Proteins) channels generate larger resurgent currents than human Nav1.1 (show SCN1A Proteins) channels, but the SCN4B-derived Navbeta4 peptide does not protect either isoform from use-dependent reduction.
In a nonreferred nationwide Danish cohort of SIDS (show IDS Proteins) cases, up to 5/66 (7.5%) of SIDS (show IDS Proteins) cases can be explained by genetic variants in the sodium channel complex genes.
this is the first study to demonstrate an association of SCN4B mutations with AF, suggesting SCN4B as a novel AF susceptibility gene.
SCN5A (show SCN5A Proteins)-SCN4B were found to be essential for positive selection of CD4 (show CD4 Proteins)(+) T cells.
The researchers found evidence of an association between SCN4B subunit mutations and sudden infant death syndrome pathogenesis.
The paroxysmal extreme pain disorder associated Nav1.7 (show SCN9A Proteins) missense mutations M1627K, T1464I and V1299F increase Navbeta4 peptide-mediated resurgent sodium currents, in contrast to the erythromelalgia associated I848T and L858H Nav1.7 (show SCN9A Proteins) missense mutations.
SCN4B is a long QT syndrome susceptibility gene.
The protein encoded by this gene is one of several sodium channel beta subunits. These subunits interact with voltage-gated alpha subunits to change sodium channel kinetics. The encoded transmembrane protein forms interchain disulfide bonds with SCN2A. Defects in this gene are a cause of long QT syndrome type 10 (LQT10). Three protein-coding and one non-coding transcript variant have been found for this gene.
sodium channel accessory subunit
, sodium channel beta 4 subunit
, sodium channel subunit beta-4
, sodium channel, type IV, beta polypeptide
, voltage gated sodium channel beta 4 subunit
, sodium channel, type 4, beta subunit
, sodium channel, type IV, beta