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- Table of Contents
Facts about Sodium channel subunit beta-4.
Modulates the susceptibility of the sodium channel to inhibition by toxic peptides from spider, scorpion, wasp and sea anemone venom. .
Human | |
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Gene Name: | SCN4B |
Uniprot: | Q8IWT1 |
Entrez: | 6330 |
Belongs to: |
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sodium channel auxiliary subunit SCN4B (TC 8.A.17) family |
sodium channel beta-4 subunit; sodium channel subunit beta-4; sodium channel, voltage-gated, type IV, beta
Mass (kDA):
24.969 kDA
Human | |
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Location: | 11q23.3 |
Sequence: | 11; NC_000011.10 (118133377..118152823, complement) |
Expressed at a high level in dorsal root ganglia, at a lower level in brain, spinal cord, skeletal muscle and heart. Expressed in the atrium.
Cell membrane; Single-pass type I membrane protein.
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The SCN4B gene is a candidate for mutation in the LQTS susceptibility gene. This mutation has many advantages. The L179F variant causes an 8 or 3-fold increase of the late-sodium current. This supports the idea that the SCN4B mutation encodes a new susceptibility genetic for LQTS. A mutational analysis of four sodium channels alpha subunits was done (Na(vbeta),). The missense mutation L179F (C535T), was found in SCN4B. This mutation was generated by site-directed mutantgenesis and expressed on human HEK293 cell lines.
The SCN4B gene codes a subunit for the voltage-gated sodium channel NaVb4. The subunit is found in the nervous system, in particular in restricted brain areas and in skeletal muscles cells. It shares a similar sequence to the NaVb2 Subunit and both encoding proteins interact with NaVa. These interactions regulate the activity of NaVa subunits. The SCN4B Subunit has been implicated in cell-cell adhesion, neurite extension and persistent sodium currents in neurons.
Induction of tLTD is dependent on the cellular expression of Scn4b in NAc medium spiny cells. It is involved the modulation of dendritic Calcium transients evoked from backpropagating.APs. In addition, the SCN4B marker regulates the induction of tLTD in NAc medium spiny neurons. This marker is useful in many areas of neuroscience, as it can be used to identify the cells that are essential for the maintenance and stimulation of synaptic plasticity.
Normal mammary epithelial cells have high levels of NaVb4 proteins, and some subunits may be upregulated in cancers. In cancer samples, NaVb4 protein is always downregulated. This subunit has been identified in colorectal cancer, prostate cancer, and breast cancer. Studies have also shown that the SCN4B gene is linked to metastasis suppression. These results are specific to one type of cell and cannot be applied to other types of tumors.
The SCN4B gene encodes a transmembrane protein called the sodium channel beta-4 (SCN4B). The SCN4B subunit is expressed in all neurons in the brain. However, the subunits in sodium channels are different in different tissues, such as the brain. A subunit called the "b4" subunit is highly expressed within the dorsal Striata and confers unique gate properties.
Anti-SCN4B antibodies are available from many suppliers and target the SCN4B gene. The protein, which is 25 kilodaltons in mass, is a sodium voltage-gated channel beta subunit. The antibody might also recognize orthologs found in mice, canines and monkeys. Studies have shown that certain types of cancer can be caused by the SCN4B protein.
The SCN4B protein encodes the NaVb4 Subunit. It can be found in the nervous systems and restricted skeletal muscle cells. Its amino acid sequence is homologous to the NaVb2 Subunit, which engages with NaVa in covalent interactions. The SCN4B gene is also implicated in sodium channel activity and regulation of cell-cell adhesion, neurite extension, and vascular tone.
MCF10A, pcDNA3.1, and MDA–MB-231 cells expressed the NaVb4 gene. It was found that breast cancer and prostate carcinoma had lower levels of NaVb4 proteins. This marker was also associated with expression of mesenchymal markers. The SCN4B gene has been implicated as a cancer metastasis-suppressor.
Multiple mutations have been identified within the SCN4B gene. These mutations all localize to the extracellular domain of the protein, which is essential for its gating properties. They were all found in GEFS+ individuals. The most common mutation causes temporal lobe epilepsy and febrile seizures. Many aspects of epilepsy are influenced by the SCN4B genes. The SCN4B mutant causes persistent inactivation and inactivation of sodium channels.
In a separate study, this marker was also identified as a possible RGC subset marker. It was found to be in approximately 10% percent of clusters, which is a strong indication of its utility as a subset marker. This new discovery could help us identify a distinct subset RGCs in murine retina. It is also an important tool to further study the CNS. It could be used to help us understand the mechanisms behind labeling different types neurons.
Patients with cardiac arrhythmias should have the SCN4B mark available. This gene is found in the heart and is associated with a variety of disorders, including long QT syndrome type 3 and Brugada syndrome. The gene contributes to atrial stoppage, drug-induced Torsades de Pointes, and sudden Infant Death Syndrome.
The SCN4B gene is an important tool in neuroimaging as well as therapeutics. Its mutation has been associated to a range pain conditions, including mechanical, inflammatory, thermal, and inflammatory. This suggests that the channel could be a target for analgesics or narcotics because of the association between SCN4B mutations with pain. It is not known if this gene is involved in the process, but it is likely.
PMID: 12930796 by Yu F.H., et al. Sodium channel beta4, a new disulfide-linked auxiliary subunit with similarity to beta2.
PMID: 24297919 by Gilchrist J., et al. Crystallographic insights into sodium-channel modulation by the beta4 subunit.