Sodium Channel, Voltage-Gated, Type I, alpha Subunit Proteins (SCN1A)

The vertebrate sodium channel is a voltage-gated ion channel essential for the generation and propagation of action potentials, mainly in nerve and muscle. Additionally we are shipping Sodium Channel, Voltage-Gated, Type I, alpha Subunit Antibodies (24) and many more products for this protein.

list all proteins Gene Name GeneID UniProt
Mouse SCN1A SCN1A 20265  
Rat SCN1A SCN1A 81574 P04774
SCN1A 6323 P35498
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Top Sodium Channel, Voltage-Gated, Type I, alpha Subunit Proteins at antibodies-online.com

Showing 2 out of 5 products:

Catalog No. Origin Source Conjugate Images Quantity Supplier Delivery Price Details
HOST_Escherichia coli (E. coli) Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 30 to 35 Days
$4,331.68
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Insect Cells Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 50 Days
$5,442.50
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SCN1A Proteins by Origin and Source

Origin Expressed in Conjugate
Human ,

More Proteins for Sodium Channel, Voltage-Gated, Type I, alpha Subunit (SCN1A) Interaction Partners

Mouse (Murine) Sodium Channel, Voltage-Gated, Type I, alpha Subunit (SCN1A) interaction partners

  1. Pharmological manipulation by clobazam, a common anticonvulsant with preferential affinity for the GABRA2 (show GABRA2 Proteins) receptor, revealed dose-dependent protection against hyperthermia-induced seizures in Scn1a+/- mice. These findings support Gabra2 (show GABRA2 Proteins) as a genetic modifier of the Scn1a+/- mouse model of Dravet syndrome.

  2. In this study, we characterized the behavior of heterozygous mice expressing the SCN1A R1648H mutation (Scn1a(RH/+)) and the effect of stress on spontaneous and induced seizures. We also examined the effect of the R1648H mutation on the hypothalamic-pituitary-adrenal (HPA (show HPSE Proteins)) axis response.

  3. findings establish an unexpected role for Nav1.1 channels in regulating the excitability of sensory nerve fibres that mediate mechanical pain

  4. Deletion of Nav1.1 channels selectively impairs excitability of GABAergic interneurons

  5. Results show Nav1.1 haploinsufficiency in excitatory neurons has an ameliorating effect on the pathology of Dravet syndrome.

  6. These results establish a direct role for SCN1A in the regulation of sleep

  7. Loss of NaV1.1 channels in forebrain GABAergic neurons is both necessary and sufficient to cause epilepsy and premature death in Dravet syndrome.

  8. mice with Scn1a haploinsufficiency exhibit hyperactivity, stereotyped behaviours, social interaction deficits and impaired context-dependent spatial memory; results demonstrate a critical role for Na(V)1.1 channels in neuropsychiatric functions and provide a potential therapeutic strategy for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome

  9. These results demonstrate increased expression levels of Nav1.7 (show SCN9A Proteins), Nav1.8 (show SCN10A Proteins), and perhaps Nav1.1 in the dorsal root ganglia in mice with a heterozygous mutation of the Nf1 (show NF1 Proteins) gene

  10. Na(V)1.1 channels are expressed in the suprachiasmatic nucleus (SCN (show SRI Proteins)) of the hypothalamus.

Human Sodium Channel, Voltage-Gated, Type I, alpha Subunit (SCN1A) interaction partners

  1. genetic variants in 3'UTR of SCN1A

  2. Among these transmissions were two likely disease-causing mutations: an SCN1A mutation transmitted to an SUDC proband and her sibling with Dravet syndrome, as well as an SLC6A1 mutation in a proband with epileptic encephalopathy.

  3. study presents a phenotype-genotype correlation for SCN1A; described a distinct SCN1A phenotype, early infantile SCN1A encephalopathy, which is readily distinguishable from the Dravet syndrome and genetic epilepsy with febrile seizures plus

  4. This study demonstrated that early-life prolonged FSs have a profound long-term impact on neuronal function and adult seizure phenotypes in a mouse model of human SCN1A dysfunction.

  5. this study showed that SCN1A testing be considered in all individuals with febrile seizures or Dravet syndrome , as well as in familial cases consistent with febrile seizures.

  6. This study found significant differences in the distribution of truncating and missense variants across the SCN1A sequence among healthy individuals, patients with Dravet syndrome.

  7. SCN1A mutations may alter axonal function, causing motor neuropathy/neuronopathy. This may contribute to gait disturbance and orthopedic misalignment, which is characteristic of patients with Dravet syndrome.

  8. The association study indicated that age at first seizure and frameshift mutations of SCN1A were associated with Dravet syndrome.

  9. Study reported the range of rare copy number variants found in SCN1A gene in a series of Welsh patients with childhood-onset epilepsy and intellectual disability and identified clearly or likely pathogenic CNVs in 8.8 % of the patients including 5 rare de novo deletions.

  10. Our findings suggest that SCN1A mutation leads to changes in the dopamine system that may contribute to the behavioral abnormalities in DS.

Sodium Channel, Voltage-Gated, Type I, alpha Subunit (SCN1A) Protein Profile

Protein Summary

The vertebrate sodium channel is a voltage-gated ion channel essential for the generation and propagation of action potentials, mainly in nerve and muscle. Voltage-sensitive sodium channels are heteromeric complexes consisting of a large central pore-forming glycosylated alpha subunit, and two smaller auxiliary beta subunits. This gene encodes the large alpha subunit, and mutations in this gene have been associated with several epilepsy, convulsion and migraine disorders. Alternative splicing results in multiple transcript variants. The RefSeq Project has decided to create four representative RefSeq records. Three of the transcript variants are supported by experimental evidence and the fourth contains alternate 5' untranslated exons, the exact combination of which have not been experimentally confirmed for the full-length transcript.

Gene names and symbols associated with SCN1A

  • sodium channel, voltage-gated, type I, alpha subunit (SCN1A)
  • sodium channel, voltage-gated, type IX, alpha subunit (SCN9A)
  • sodium channel, voltage-gated, type I, alpha (Scn1a)
  • B230332M13 protein
  • EIEE6 protein
  • FEB3 protein
  • FEB3A protein
  • FHM3 protein
  • GEFSP2 protein
  • HBSCI protein
  • NAC1 protein
  • Nav1.1 protein
  • SCN1 protein
  • SCN1A protein
  • SCN9A protein
  • SMEI protein

Protein level used designations for SCN1A

sodium channel, voltage-gated, type IX, alpha subunit , voltage-gated sodium channel I , sodium channel, voltage-gated, type I, alpha subunit , sodium channel protein brain I subunit alpha , sodium channel protein type 1 subunit alpha , sodium channel protein type I subunit alpha , sodium channel protein, brain I subunit alpha , sodium channel voltage-gated type I alpha polypeptide , sodium channel, voltage-gated, type 1, alpha polypeptide , sodium channel, voltage-gated, type I, alpha polypeptide , voltage-gated sodium channel subunit alpha Nav1.1 , sodium channel protein, brain I alpha subunit , sodium channel voltage gated type 1 alpha subunit , sodium channel voltage-gated type I alpha

GENE ID SPECIES
100052059 Equus caballus
395946 Gallus gallus
20265 Mus musculus
81574 Rattus norvegicus
6323 Homo sapiens
478775 Canis lupus familiaris
529590 Bos taurus
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