SCN1B Antibodies

Sodium channel subunit beta-1 (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 NFASC may target the sodium channels to the nodes of Ranvier of developing axons and keep these channels at the nodes in mature myelinated axons. .

Gene Information

Human
Gene Name:	SCN1B
Uniprot:	Q07699
Entrez:	6324

Family

Belongs to:
sodium channel auxiliary subunit SCN1B (TC 8.A.17) family

Alternative Names

Sodium channel subunit beta-1

Molecular Weight

Mass (kDA):
24.707 kDA

Genomic Context

Human
Location:	19q13.11
Sequence:	19; NC_000019.10 (35030470..35040449)

Tissue Specificity

The overall expression of isoforms 1 and 2 is very similar. Isoform 1 is abundantly expressed in skeletal muscle, heart and brain. Isoform 2 is highly expressed in brain and skeletal muscle and present at a very low level in heart, placenta, lung, liver, kidney and pancreas. In brain, isoform 2 is most abundant in the cerebellum, followed by the cerebral cortex and occipital lobe, while isoform 1 levels are higher in the cortex compared to the cerebellum. Isoform 2 is expressed in many regions of the brain, including cerebellar Purkinje cells, cortex pyramidal neurons and many of the neuronal fibers throughout the brain (at protein level). Also detected in dorsal root ganglion, in fibers of the spinal nerve and in cortical neurons and their processes (at protein level).

Subcellular Localizations

[Isoform 1]: Cell membrane; Single-pass type I membrane protein. Perikaryon. Cell projection. Cell projection, axon. Detected at nodes of Ranvier on the sciatic nerve.; [Isoform 2]: Perikaryon. Cell projection. Secreted. Detected on Purkinje cells and their cell projections and on neuronal cell projections.

Interacting Proteins

• SCN4A

PTMs

• Disulfide bond

• Glycoprotein

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SCN1B

Best Uses Of The SCN1B Marker

This article will help you learn more about the SCN1B gene. This article offers valuable tips and tricks to improve your experiments. These tips and tricks will allow you to enhance the outcomes of your experiments. However, every researcher is faced with certain challenges during their experiments. While proper controls can eliminate the majority of these causes However, it is possible to encounter certain issues. These guides will help you determine the root cause of your problems.

Boster Bio FAQ

The SCN1B marker is widely used in a variety of biological tests. It reacts with various animal samples, both monoclonal as well as polyclonal. Boster Bio uses mouse and rabbit tissues to create SCN1B antibodies. The heterotrimeric sodium channel complex is dependent on the SCN1B marker. This protein is capable of modulating multiple alpha subunits. It is located in the developing axons.

Optimization

Boster Bio's ability to optimize experiments is among its strongest strengths. There are a range of choices that can be made to improve your research, including flow processes. In addition to Boster's cutting-edge analysis and reporting capabilities, its comprehensive blog and technical resources allow researchers to stay up date with the latest developments in the field. Boster's high-quality buffers for lysis help reduce the intensity of cross-linking and guarantee the highest quality of results.

Immunohistochemistry is a very popular method to detect antigens inside cells. It is based on the idea that antigens are bound to antibodies. The process involves preparation of the sample comprising fixation, embedding, and slicing. Boster Bio's Immunohistochemistry protocol provides step-by-step instructions and quick primers and reference guides. Each step includes a section that provides the best method to perform the test.

Histology

Neurotransmitter neuronal exitability is dependent on the SCN1B gene. Normal electrical excitability in humans is possible with one functional allele. We identified a variant SCN1B with a c.308A>T allele from his father and a POLR1C > allele (c.614C>T) from his mother. The child had a complex clinical picture, and was found to be mediated by an SCN1B gene variant.

A heterozygous C-to-A transversion of exon 3 of SCN1B causes the deletion of 5 amino acids from the extracellular immunoglobulin-like fold the protein. In this case, the proband had absence seizures, but no fever. Four other family members, including the proband, had febrile seizures. Another family member was affected by the same SCN1B mutation.

The highest expression of Scn1B was found in the cerebellum and hippocampus. In the majority of regions, SCN1B complements Scn3b (608214) in vivo, but this was not the case for the hippocampus. However, Morgan et al. Morgan et al. found that rats Scn1b+ mice were not more susceptible to seizures.

SCD is associated with mutations in SCN1B. These two proteins are essential for maintaining normal electrical function in hippocampus. A mutation in the SCN1B gene results in a shorter QT time in the patient. Furthermore, the HCN1C gene is associated with SCD. The inheritance is dominant in the sporadic cases and recessive in the inheritable cases.

The SCN1B gene is an essential component of the conduction system of the ventricular. Its expression is regulated by the HEY2 locus. It regulates SCN5A expression and consequently influences the rate of cardiac conduction. The mutation affects the closure of the Na+ channel, thus resulting in decreased cardiac excitability. The mutation in the SCN5A gene is also associated with Brugada syndrome.