anti-Sodium Channel, Voltage-Gated, Type IV, alpha Subunit (SCN4A) Antibodies

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. Additionally we are shipping SCN4A Proteins (10) and many more products for this protein.

list all antibodies Gene Name GeneID UniProt
SCN4A 110880 Q9ER60
SCN4A 6329 P35499
SCN4A 25722 P15390
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Top anti-SCN4A Antibodies at antibodies-online.com

Showing 10 out of 18 products:

Catalog No. Reactivity Host Conjugate Application Images Quantity Supplier Delivery Price Details
Human Rabbit Un-conjugated WB Western blot analysis of Nav1.4 expression in MCF7 (A), NIH3T3 (B), H9C2 (C), mouse brain (D) whole cell lysates. 200 μL Log in to see 13 to 14 Days
$487.50
Details
Human Rabbit Un-conjugated ELISA, ICC, IF, WB ABIN6275577 staining Hela by IF/ICC. The sample were fixed with PFA and permeabilized in 0.1% Triton X-100,then blocked in 10% serum for 45 minutes at 25¡ãC. The primary antibody was diluted at 1/200 and incubated with the sample for 1 hour at 37¡ãC. An Alexa Fluor 594 conjugated goat anti-rabbit IgG (H+L) Ab, diluted at 1/600, was used as the secondary antibod 100 μL Log in to see 11 to 12 Days
$390.77
Details
Human Rabbit Un-conjugated ELISA, WB   100 μg Log in to see 2 to 3 Days
$302.50
Details
Human Rabbit Un-conjugated ELISA, WB   100 μg Log in to see 2 to 3 Days
$302.50
Details
Human Rabbit Un-conjugated WB   100 μL Log in to see 11 to 14 Days
$375.83
Details
Human Rabbit Un-conjugated WB   100 μL Log in to see 11 to 14 Days
$522.50
Details
Human Rabbit Un-conjugated IHC, WB   100 μL Log in to see 7 to 8 Days
$454.67
Details
Human Rabbit Un-conjugated IHC, WB   100 μL Log in to see 11 to 14 Days
$551.83
Details
Human Rabbit Un-conjugated EIA, IHC (fro), WB   0.2 mL Log in to see 6 to 8 Days
$500.50
Details
Human Rabbit Un-conjugated ELISA, WB   100 μg Log in to see 11 to 16 Days
$312.70
Details

More Antibodies against SCN4A Interaction Partners

Mouse (Murine) Sodium Channel, Voltage-Gated, Type IV, alpha Subunit (SCN4A) interaction partners

  1. NaV1.4 null mice have latent myasthenia and a right shift of the force-stimulus relation, without evidence of periodic paralysis. Sodium current density was half that of wild-type muscle and no compensation by retained expression of the foetal NaV1.5 isoform was detected. Mice null for NaV1.4 did not survive beyond the second postnatal day.

  2. In-depth characterization of draggen mice uncovered novel systemic metabolic abnormalities in Scn4a mouse models and provided novel insights into disease mechanisms

  3. HyperKPP phenotype does not depend solely on the NaV1.4 content.

  4. Homozygous R669H mice had a robust hypokalemic periodic paralysis phenotype, with transient loss of muscle excitability and weakness in low-K+ challenge, insensitivity to high-K+ challenge, dominant inheritance, and absence of myotonia.

  5. A distinct autosomal recessive myotonic mouse in the C57BL/6 background (line B6MT)is reported in which the Scn4a gene shows polymorphism with no functional consequences.

  6. The skeletal muscle isoform of Na(v)1.4, which represents over 90% of voltage-gated sodium channels in muscle, plays an important role in development of abnormally high Na(+) concentrations found in muscle from mdx mice.

Human Sodium Channel, Voltage-Gated, Type IV, alpha Subunit (SCN4A) interaction partners

  1. this study reports the cryo-electron microscopy structure of the human Nav1.4-beta1 complex at 3.2-A resolution.

  2. R1451 pathogenic mutations shifted the inactivation kinetics and reduced the current density.

  3. structural basis for gating pore current in periodic paralysis; results reveal pathogenic mechanisms of periodic paralysis at the atomic level and suggest designs of drugs that may prevent ionic leak and provide symptomatic relief from hypokalaemic and normokalaemic periodic paralysis

  4. Rare SCN4A variants that directly alter NaV1.4 function occur in infants who had died from SIDS. These variants are predicted to significantly alter muscle membrane excitability and compromise respiratory and laryngeal function.

  5. We report on 3 brothers presenting a peculiar clinical and histopathologic phenotype characterized by facial weakness with ptosis and a mild dystrophic pattern associated with recessive SCN4A mutations.

  6. Paramyotonia congenita-causing mutation N1366S leads to a gain-of-function change of NaV1.4 gating in response to cold.

  7. Data suggest that mutation of the sodium channel, voltage-gated, type IV, alpha protein (SCN4A) gene probably underlies the hypokalemic periodic paralysis in the family.

  8. We identified a novel Nav 1.4 mutation I692M in 14 families out of the 104 genetically identified Hyperkalemic periodic paralysis (HyperPP) families in the Neuromuscular Centre Ulm and is therefore as frequent as I693T (13 families out of 14 HyperPP families) in Germany. Surprisingly, in 13 families, a known polymorphism S906T was also present

  9. Combining our results with the literature on Chinese populations indicates that 21 mutations in CLCN1 have been associated with myotonia congenital, while 7 mutations in SCN4A have been associated with paramyotonia congenita, 2 mutations in SCN4A have been associated with sodium channel myotonias.

  10. A rare variant p.Pro1629Leu in SCN4A identified in a patient with a skeletal muscle deficit and intermittent dysphagia.

  11. Cohort of 30 patients carrying the c.3466G>A p.A1156T mutation in the SCN4A gene showed a consistent phenotype of predominant myalgia, muscle stiffness, and exercise cramps without signs of clinical myotonia, paramyotonia, or periodic paralyses; modest gain in the function of p.A1156T channel in whole-cell patch clamp studies may explain the absence of clinical myotonia

  12. These data suggest a possible involvement of SCN4A variants in the pathophysiological mechanism underlying the development of a spontaneous or drug-induced type 1 electrocardiographic pattern and the occurrence of malignant arrhythmias in some patients with Brugada syndrome.

  13. association of the genetic variability of SCN4A with the development of essential tremor

  14. Computer simulations of the effects of the I693T mutation were introduced in the muscle fiber model by both hyperpolarizing shifts in the Nav1.4 channel activation and a faster recovery from slow channel inactivation

  15. CACNA1S and SCN4A mutations are relatively rare in patients with hypokalemic periodic paralysis

  16. Recessive loss-of-function SCN4A mutations were identified in congenital myopathy patients.

  17. The c.4427 T>C (p.Met1476Thr) mutation of the SCN4A gene contribute to the paramyotonia congenita.

  18. Mutation analysis in the patient and in child's mother revealed a heterozygous p.N1180I mutation in exon 19 of SCN4A gene. In newborns with stiffness, peripheral contractures and myotonia, the sequence analysis of SCN4A gene should be performed.

  19. As the result, heterozygous mutations c.2024G>A (R675Q) and c.1333G>A (V445M) of gene SCN4A were identified in the hypokalemic periodic paralysis patient and the paramyotonia congenita family respectively.

  20. The patient with scn4a mutation exhibited various symptoms that evolved with age, including apneic episodes, tonic muscular contractions during sleep, fluctuating severe episodic myotonia, and finally episodic paralyses.

SCN4A Antigen Profile

Protein Summary

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel alpha subunit gene family. It is expressed in skeletal muscle, and mutations in this gene have been linked to several myotonia and periodic paralysis disorders.

Gene names and symbols associated with SCN4A

  • sodium channel, voltage-gated, type IV, alpha (Scn4a) antibody
  • sodium voltage-gated channel alpha subunit 4 (SCN4A) antibody
  • sodium voltage-gated channel alpha subunit 4 (Scn4a) antibody
  • sodium channel, voltage-gated, type IV, alpha, b (scn4ab) antibody
  • HOKPP2 antibody
  • HYKPP antibody
  • HYPP antibody
  • mH2 antibody
  • microI antibody
  • Na(V)1.4 antibody
  • NAC1A antibody
  • Nav1.4 antibody
  • Nav1.4b antibody
  • NCHVS antibody
  • SkM1 antibody

Protein level used designations for SCN4A

sodium channel alpha-subunit , sodium channel protein skeletal muscle subunit alpha , sodium channel protein type 4 subunit alpha , sodium channel protein type IV subunit alpha , sodium channel, voltage-gated, type IV, alpha polypeptide , voltage-gated sodium channel subunit alpha Nav1.4 , skeletal muscle voltage-dependent sodium channel type IV alpha subunit , Sodium channel voltage-gated type IV alpha polypeptide , mu-1 , skM1 , sodium channel voltage-gated type 4 alpha polypeptide , sodium channel, voltage-gated, type 4, alpha polypeptide , sodium channel, voltage-gated, type 4, alpha subunit , sodium channel, voltage-gated, type IV, alpha subunit , Sodium channel protein skeletal muscle subunit alpha , Sodium channel protein type IV subunit alpha , Voltage-gated sodium channel subunit alpha Nav1.4 , skeletal muscle sodium channel alpha-subunit , sodium channel protein type 4 subunit alpha-like , Nav1.4b , Voltage-gated sodium channel subunit alpha Nav1.4b , sodium channel protein type 4 subunit alpha B , voltage-gated sodium channel subunit alpha Nav1.4b , zscn5

GENE ID SPECIES
110880 Mus musculus
6329 Homo sapiens
25722 Rattus norvegicus
610754 Canis lupus familiaris
718194 Macaca mulatta
100049793 Equus caballus
100414137 Callithrix jacchus
100450057 Pongo abelii
100470881 Ailuropoda melanoleuca
100511715 Sus scrofa
100612017 Pan troglodytes
564977 Danio rerio
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