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- Table of Contents
Facts about Sodium channel protein type 1 subunit alpha.
Plays a key role in brain, probably by modulating the moment when neurotransmitters are released in neurons. Involved in sensory perception of mechanical pain: activation in somatosensory neurons induces pain without neurogenic inflammation and produces hypersensitivity to mechanical, but not thermal stimulation.
Human | |
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Gene Name: | SCN1A |
Uniprot: | P35498 |
Entrez: | 6323 |
Belongs to: |
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sodium channel (TC 1.A.1.10) family |
Sodium channel protein type 1 subunit alpha
Mass (kDA):
228.972 kDA
Human | |
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Location: | 2q24.3 |
Sequence: | 2; NC_000002.12 (165984641..166149161, complement) |
Cell membrane; Multi-pass membrane protein.
You've likely noticed lots of buzz about the SCN1A Marker when you've been following Encoded Therapeutics and Boster Bio. What exactly is SCN1A and what can it do in your research? In this article, we'll talk about Scn1a and the Incubation of the SCN1A Marker.
Boster Bio's SCN1A antibody is one of the primary antibodies that react with human, mouse and the rat cells. This antibody is stable at -20°C for 6 months. It contains 5mg BSA as well as an peptide sequence that can be purchased separately. You can also purchase a blocking protein to prevent your antibody from binding to SCN1A.
Gene therapy is possible using the SCN1A gene. This therapy is designed to increase the production of SCN1A protein in patients with Dravet syndrome. Encoded Therapeutics is working on this gene therapy. The company integrated DNA into an AAV vector to increase the production of SCN1A protein. The company offers additional products to treat this disease, in addition to gene therapy.
SCN1A can be found in nearly all mammals. As part of the Picoband(TM) catalog, Boster Bio has an antibody that targets SCN1A. The antibody reacts with mouse, human and rat proteins. This product is stored at -20degC for up to six months. It also contains 5 mg of BSA and the peptide sequence, which can be purchased separately.
The SCN1A gene encodes a sodium channel that is voltage-gated, dubbed NaV1.1. SCN1A mutations cause Dravet Syndrome which is a severe form of epilepsy that is common in children. This gene causes a reduction in the excitability of inhibitory neurons due to functional mutations. This reduced activity of the channel can cause other network changes. The Hm1a gene was used to investigate the CA1 microcircuit and the pyramidal excitatory neuron.
The SCN1A gene is a clinically relevant epilepsy gene. Around 10% of GEFS+ cases are affected by mutations in SCN1A. The etiology for about twenty-three percent of DS is not yet known. In this study, the mother's SCN1A gene was found to have abnormalities in exons 8 to 16. The mother was mosaic and had a CNV in at least one gene.
The mutations in SCN1A in mice cause autism-like symptoms, like seizures and dysfunction of inhibitory interneurons. These discoveries were intriguing, but some mice died before being assessed for firing interneurons. Kevin Bender, an associate professor of neuroscience at the University of California San Francisco, believes that the new method of study is revolutionary.
Invitrogen has provided a codon-optimized SCN1A CDNA to achieve this result. It contained a recombination free sequence (pCMV–SCN1A) as well as two ubiquitous promoters that are the early enhancementr of the citomegalovirus and the human Extension Factor 1a. The reporter gene was the pcDNA3.1 vector. The pCAGGS vector was derived from HEK-293 cell lines at an end-limiting dilution.
SCN1A mRNA was present in the patient's neuron. The patient's mutated variant escaped decay caused by nonsense and then translated into the gene. This mutated allele was located at the end of the coding exon. The resultant mRNA could express SCN1A, and its expression was decreased. The mRNA was able to express all other reprogramming factors including NCP.
In this study, two patients suffering from Dravet syndrome carried the mutation SCN1A. The results of PCR-RFLP revealed that the SCN1A c.5347G mutation was discovered. The SCN1A mutation resulted in an even more severe condition than the control group. However, the SCN1A gene has been known to trigger seizures. Therefore, researchers looked into the relationship between SCN1A and Dravet syndrome.
The SCN1A gene is part of a family of sodium channels. The sodium channels are responsible for transferring positively charged sodium atoms into cells. They also play an important role in cell signaling. When the sodium levels are high the sodium ions are released from the adjacent neurons. These sodium ions allow neurotransmitters to reach their goals. This makes sodium ions an essential component of neurotransmitters.
PMID: 10742094 by Escayg A., et al. Mutations of SCN1A, encoding a neuronal sodium channel, in two families with GEFS+2.
PMID: 8062593 by Malo M.S., et al. Localization of a putative human brain sodium channel gene (SCN1A) to chromosome band 2q24.
*More publications can be found for each product on its corresponding product page