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Sodium Channel, Voltage-Gated, Type I, beta (SCN1B) ELISA Kits

Voltage-gated sodium channels are heteromeric proteins that function in the generation and propagation of action potentials in muscle and neuronal cells. Additionally we are shipping Sodium Channel, Voltage-Gated, Type I, beta Antibodies (63) and Sodium Channel, Voltage-Gated, Type I, beta Proteins (9) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
Anti-Mouse SCN1B SCN1B 20266 P97952
Anti-Rat SCN1B SCN1B 29686 Q00954
Anti-Human SCN1B SCN1B 6324 Q07699
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More ELISA Kits for Sodium Channel, Voltage-Gated, Type I, beta Interaction Partners

Mouse (Murine) Sodium Channel, Voltage-Gated, Type I, beta (SCN1B) interaction partners

  1. Loss of Scn1b caused increased amplitude of tetrodotoxin-sensitive INa (show INA ELISA Kits), delayed after-depolarizations, triggered beats, changed Ca2 (show CA2 ELISA Kits)+ transients,and susceptibility ventricular arrhythmias.

  2. 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

  3. Scn1b mutant subicular and layer 2/3 pyramidal neurons had increased action potential firing rates, presumably as a consequence of their increased input resistance

  4. Stronger expressions of SCN5a (show SCN5A ELISA Kits), SCN1b and Kir2.1 (show KCNJ2 ELISA Kits) were observed in ventricular-like and atrial-like cells compared to that of pacemaker-like cardiomyocytes.

  5. Scn1b is critical for neuronal proliferation, migration, and pathfinding during the critical postnatal period of brain development.

  6. The results presented here identify Navbeta1 as a component of native neuronal Kv4.2 (show KCND2 ELISA Kits)-encoded I(A) channel complexes and a novel regulator of I(A) channel densities and neuronal excitability.

  7. Scn1b regulates the electrical excitability of nociceptive DRG neurons in vivo by modulating both I(Na) and I(K).

  8. 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

  9. 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 (show SCN3A ELISA Kits), and Na(v)1.6 plus beta1 and/or beta3 subunits in the transverse tubules.

  10. Floxed allele for conditional inactivation of the voltage-gated sodium channel beta1 subunit Scn1b.

Human Sodium Channel, Voltage-Gated, Type I, beta (SCN1B) interaction partners

  1. Contribution of Cardiac Sodium Channel (show SCN5A ELISA Kits) beta-Subunit (show POLG ELISA Kits) Variants to Brugada Syndrome.

  2. 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.

  3. In a nonreferred nationwide Danish cohort of SIDS (show IDS ELISA Kits) cases, up to 5/66 (7.5%) of SIDS (show IDS ELISA Kits) cases can be explained by genetic variants in the sodium channel complex genes.

  4. We also identified an SCN1B T189M variant in 2 probands with lone AF and in 1 of 250 control subjects.

  5. 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

  6. High SCN1B expression is associated with increased tumour growth and metastasis in breast cancer.

  7. 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.

  8. SCN1B mutation is not a common cause of Dravet syndrome.

  9. results suggest that R214Q variation in SCN1Bb is a functional polymorphism that may serve as a modifier of the substrate responsible for Brugada syndrome or SIDS (show IDS ELISA Kits) phenotypes

  10. Mutation analysis of the SCN1B, SCN1A (show SCN1A ELISA Kits) and GABRG2 (show GABRG2 ELISA Kits) genes in children affected by Genetic (Generalised) Epilepsy with Febrile Seizures plus was performed

Sodium Channel, Voltage-Gated, Type I, beta (SCN1B) Antigen Profile

Antigen Summary

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.

Gene names and symbols associated with SCN1B

  • sodium channel, voltage-gated, type I, beta (Scn1b) antibody
  • sodium channel, voltage-gated, type I, beta subunit (SCN1B) antibody
  • GEFSP1 antibody

Protein level used designations for SCN1B

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

GENE ID SPECIES
20266 Mus musculus
29686 Rattus norvegicus
6324 Homo sapiens
484584 Canis lupus familiaris
618204 Bos taurus
100009211 Oryctolagus cuniculus
747705 Pan troglodytes
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