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Voltage-gated sodium channels are heteromeric proteins that function in the generation and propagation of action potentials in muscle and neuronal cells.
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Loss of Scn1b caused increased amplitude of tetrodotoxin-sensitive INa (zeige INA Antikörper), delayed after-depolarizations, triggered beats, changed Ca2 (zeige CA2 Antikörper)+ transients,and susceptibility ventricular arrhythmias.
Study showed that Scn1b is widely expressed at axon initial segments across the mouse brain, there is considerable heterogeneity in the proportion of Scn1b-positive neurons and the amount of expression between and within brain regions
Scn1b mutant subicular and layer 2/3 pyramidal neurons had increased action potential firing rates, presumably as a consequence of their increased input resistance
Stronger expressions of SCN5a (zeige SCN5A Antikörper), SCN1b and Kir2.1 (zeige KCNJ2 Antikörper) were observed in ventricular-like and atrial-like cells compared to that of pacemaker-like cardiomyocytes.
Scn1b is critical for neuronal proliferation, migration, and pathfinding during the critical postnatal period of brain development.
The results presented here identify Navbeta1 as a component of native neuronal Kv4.2 (zeige KCND2 Antikörper)-encoded I(A) channel complexes and a novel regulator of I(A) channel densities and neuronal excitability.
Scn1b regulates the electrical excitability of nociceptive DRG neurons in vivo by modulating both I(Na) and I(K).
propose reciprocity of function between Scn1b (beta1) and Na(v)1.6 such that beta1-mediated neurite outgrowth requires Na(v)1.6-mediated I(Na), and Na(v)1.6 localization and consequent high-frequency firing require beta1
The primary sodium channels present in ventricular myocytes are composed of Na(v)1.5 plus beta2 and/or beta4 subunits in intercalated disks and Na(v)1.1, Na(v)1.3 (zeige SCN3A Antikörper), and Na(v)1.6 plus beta1 and/or beta3 subunits in the transverse tubules.
Floxed allele for conditional inactivation of the voltage-gated sodium channel beta1 subunit Scn1b.
we confirm the recessive inheritance of 2 novel SCN1B mutations in 5 children from 3 families with developmental epileptic encephalopathy. The recessive inheritance and early death in these patients is consistent with the Dravet-like phenotype observed in Scn1b(-/-) mice.
This report provides the first genetic evidence of SCN1B mutation causing the Benign Familial Infantile Epilepsy (BFIE) phenotype.
Contribution of Cardiac Sodium Channel (zeige SCN5A Antikörper) beta-Subunit (zeige POLG Antikörper) Variants to Brugada Syndrome.
SCN1B gene mutations that reduce sodium channel current may provide a mechanistic link between Atrioventricular nodal reentrant tachycardia and Brugada syndrome and predispose to expression of both phenotypes.
In a nonreferred nationwide Danish cohort of SIDS (zeige IDS Antikörper) cases, up to 5/66 (7.5%) of SIDS (zeige IDS Antikörper) cases can be explained by genetic variants in the sodium channel complex genes.
We also identified an SCN1B T189M variant in 2 probands with lone AF and in 1 of 250 control subjects.
Study showed that the human SCN1B C121W epilepsy mutation leads to decreased axon initial segments expression of SCN1B in heterozygous CW mice and a complete lack of SCN1B in homozygous WW mice
High SCN1B expression is associated with increased tumour growth and metastasis in breast cancer.
experimental data indicate that sodium channel voltage-gated type I beta subunit (Navbeta1b)/H162P results in reduced sodium channel activity functionally affecting the ventricular action potential.
SCN1B mutation is not a common cause of Dravet syndrome.
Voltage-gated sodium channels are heteromeric proteins that function in the generation and propagation of action potentials in muscle and neuronal cells. They are composed of one alpha and two beta subunits, where the alpha subunit provides channel activity and the beta-1 subunit modulates the kinetics of channel inactivation. This gene encodes a sodium channel beta-1 subunit. Mutations in this gene result in generalized epilepsy with febrile seizures plus, Brugada syndrome 5, and defects in cardiac conduction. Multiple transcript variants encoding different isoforms have been found for this gene.
sodium channel subunit beta-1
, sodium channel, voltage-gated, type I, beta polypeptide
, sodium channel voltage-gated type 1 beta polypeptide
, sodium channel voltage-gated type I beta polypeptide
, sodium channel, voltage-gated, type 1, beta polypeptide
, sodium channel beta-1 subunit
, sodium channel beta 1-subunit