Sodium channel subunit beta-1; SCN1B

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit Ig

Rabbit

This SCN1B antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 63-90 amino acids from the N-terminal region of human SCN1B.

Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab)

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.

Vial Concentration: 0.5 (lot specific)

Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C in small aliquots to prevent freeze-thaw cycles.

Small volumes of anti-SCN1B antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

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. SCN1B 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.

Metabolism; Neuroscience; Signal Transduction

Western Blot (WB), ELISA (EIA), Immunohistochemistry (IHC), Flow Cytometry (FC/FACS)

WB~~1:1000

SCN1B Antibody (N-Term) western blot analysis in mouse Neuro-2a cell line lysates (35ug/lane).This demonstrates the SCN1B antibody detected the SCN1B protein (arrow).

SCN1B Antibody (N-Term) immunohistochemistry analysis in formalin fixed and paraffin embedded human brain tissue followed by peroxidase conjugation of the secondary antibody and DAB staining. This data demonstrates the use of the SCN1B Antibody (N-Term) for immunohistochemistry. Clinical relevance has not been evaluated.

SCN1B Antibody (N-Term) flow cytometric analysis of Hela cells (right histogram) compared to a negative control cell (left histogram).FITC-conjugated goat-anti-rabbit secondary antibodies were used for the analysis.

24707

sodium channel, voltage gated, type I beta subunit

sodium channel subunit beta-1

Sodium channel subunit beta-1

SCN1B_HUMAN

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.[provided by RefSeq, Oct 2009]

SCN1B: Crucial in the assembly, expression, and functional modulation of the heterotrimeric complex of the sodium channel. The subunit beta-1 can modulate multiple alpha subunit isoforms from brain, skeletal muscle, and heart. Its association with neurofascin may target the sodium channels to the nodes of Ranvier of developing axons and retain these channels at the nodes in mature myelinated axons. Defects in SCN1B are the cause of generalized epilepsy with febrile seizures plus type 1 (GEFS+1). Generalized epilepsy with febrile seizures-plus refers to a rare autosomal dominant, familial condition with incomplete penetrance and large intrafamilial variability. Patients display febrile seizures persisting sometimes beyond the age of 6 years and/or a variety of afebrile seizure types. GEFS+ is a disease combining febrile seizures, generalized seizures often precipitated by fever at age 6 years or more, and partial seizures, with a variable degree of severity. Defects in SCN1B are the cause of Brugada syndrome type 5 (BRGDA5). 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 (called ventricular fibrillation), the individual will faint and may die in a few minutes if the heart is not reset. Belongs to the sodium channel auxiliary subunit SCN1B (TC 8.A.17) family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral; Channel, sodium

Chromosomal Location of Human Ortholog: 19q13.1

Cellular Component: voltage-gated sodium channel complex; T-tubule; extracellular region

Molecular Function: sodium channel inhibitor activity; sodium channel regulator activity; voltage-gated sodium channel activity

Biological Process: membrane depolarization; synaptic transmission; axon guidance; action potential propagation; corticospinal neuron axon guidance; cell adhesion; locomotion; response to pyrethroid; cardiac muscle contraction

Disease: Generalized Epilepsy With Febrile Seizures Plus, Type 1; Atrial Fibrillation, Familial, 13; Brugada Syndrome 5

Grover, S., et al. Pharmacogenomics 11(7):927-941(2010)
Tan, B.H., et al. Heart Rhythm 7(6):771-778(2010)
Casini, S., et al. Cardiovasc. Res. 85(4):691-700(2010)
Ogawa, R., et al. Int J Clin Pharmacol Ther 48(2):109-119(2010)
Watanabe, H., et al. Circ Arrhythm Electrophysiol 2(3):268-275(2009)

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