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Sodium Channel, Voltage-Gated, Type V, alpha Subunit (SCN5A) ELISA Kits

The protein encoded by SCN5A is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. Additionally we are shipping Sodium Channel, Voltage-Gated, Type V, alpha Subunit Antibodies (111) and Sodium Channel, Voltage-Gated, Type V, alpha Subunit Proteins (11) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
Anti-Mouse SCN5A SCN5A 20271 Q9JJV9
Anti-Human SCN5A SCN5A 6331 Q14524
Anti-Rat SCN5A SCN5A 25665 P15389
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More ELISA Kits for Sodium Channel, Voltage-Gated, Type V, alpha Subunit Interaction Partners

Mouse (Murine) Sodium Channel, Voltage-Gated, Type V, alpha Subunit (SCN5A) interaction partners

  1. Enhanced A-V conduction in mice overexpressing SCN5A in the heart mimics the human syndrome of Enhanced Atrioventricular Nodal Conduction .

  2. Loss of the C-terminus of connexin43 (show GJA1 ELISA Kits) limits microtubule plus-end capture and NaV1.5 localization at the intercalated disc.

  3. Ser571-mediated increases in INa (show INA ELISA Kits),L promote abnormal repolarization and intracellular Ca(2 (show CA2 ELISA Kits)+) handling and increase susceptibility to arrhythmia. Ser571 is required for maladaptive remodeling and arrhythmias in response to pressure overload.

  4. intracellular Ca(2 (show CA2 ELISA Kits)+) contributes to the regulation of INaL conducted by NaV1.5 mutants and propose that, during excitation-contraction coupling, elevated intracellular Ca(2 (show CA2 ELISA Kits)+) suppresses mutant channel INaL and protects cells from delayed repolarization.

  5. Results show that Nav1.5 upregulation correlates with disease severity in monophasic and chronic-relapsing experimental autoimmune encephalomyelitis and that Nav1.5 expression in astrocytes is modulated in parallel with periods of disease and remission

  6. FoxO1 (show FOXO1 ELISA Kits) is involved in the modulation of NaV1.5 expression in ischemic heart disease.

  7. Our results suggested that the main expression subtype of sodium channels was Nav1.5 of early embryonic cardiomyocytes.

  8. Data indicate that reduction in connexin43 (Cx43) and sodium channel NaV1.5 expression coincided with overexpression of transgene calcineurin A (CnA) and hypertrophy development and preceded significant presence of fibrosis.

  9. Expression of NaV1.5 in cardiomyocytes is regulated by the PDZ domain (show INADL ELISA Kits)-binding motif.

  10. Analysis of BAC transgenic strains harboring an engineered deletion of the enhancer within Scn10a (show SCN10A ELISA Kits) revealed that the enhancer was essential for Scn5a expression in cardiac tissue. SCN10A (show SCN10A ELISA Kits) variant rs6801957 modulated Scn5a expression in the heart.

Human Sodium Channel, Voltage-Gated, Type V, alpha Subunit (SCN5A) interaction partners

  1. Compound heterozygous variants c.101G>A and c.3832G>A in the SCN5A gene were found in the complete heart block affected child and were not found in unaffected family members.

  2. the mutantinduced changes contributed to the loss of function of Nav1.5 channels, which indicates that the p.D1690N variant may have a pathogenic role in Brugada syndrome.

  3. This initial functional study for SCN5A mutation in the Chinese SUNDS victim revealed that the acidosis aggravated the loss of function of mutant channel R1512W

  4. Nav1.5 N-terminal domain binding to alpha1-syntrophin (show SNTA1 ELISA Kits) increases membrane density of human Kir2.1 (show KCNJ2 ELISA Kits), Kir2.2 (show KCNJ12 ELISA Kits) and Nav1.5 channels

  5. p.Gln1507-Lys1508-Pro1509del mutation, p.Arg222Ter nonsense mutation, and p.Met1498Arg mutation in the SCN5A gene in long-QT syndrome type 3, Brugada syndrome, and sick sinus syndrome, respectively, were found in the Iranian population.

  6. We investigated the frequency of the p.R1193Q substitution in > 4000 genomic DNA samples from 34 Asian, European, and African populations using TaqMan and/or APLP (show APLP1 ELISA Kits) (amplified product length polymorphism) assays. Allele A (p.1193Q) was detected in most Asian populations, but was sporadically observed or absent in European and African populations. These results demonstrated that the p.R1193Q substitution is character

  7. The present study demonstrated that a novel heterozygous missense mutation of A1055G in SCN5A led to 'loss-of function' of the sodium channels, and we suggest that it accounts for the arrhythmogenic characteristics of ERS.

  8. Identifies alphaB-crystallin as a new binding partner for Nav1.5. alphaB-Crystallin interacts with Nav1.5 and increases INa by modulating the expression level and internalization of cell surface Nav1.5 and ubiquitination of Nav1.5, which requires the protein-protein interactions between alphaB-crystallin and Nav1.5 and between alphaB-crystallin and functionally active Nedd4-2.

  9. The p.R1309H homozygous NaV1.5 mutation conferred both gain-of-function and loss-of-function effects on NaV1.5 channel activity. Reduction of a mutation-induced gating pore current by lidocaine suggested a therapeutic mechanism

  10. SCN5A genetic variants are linking to different cardiomyopathies (Review)

Rabbit Sodium Channel, Voltage-Gated, Type V, alpha Subunit (SCN5A) interaction partners

  1. Freshly dispersed rabbit airway smooth muscle cells express a fast voltage-gated Na(+) current that is mediated mainly by the NaV1.5 subtype.

  2. Mechanisms are determined by a two-dimensional slice model at single-cell and tissue levels in order to determine that SCN5A mutations impair cardiac pacemaking.

Sodium Channel, Voltage-Gated, Type V, alpha Subunit (SCN5A) Antigen Profile

Antigen Summary

The protein encoded by this gene is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. This protein is found primarily in cardiac muscle and is responsible for the initial upstroke of the action potential in an electrocardiogram. Defects in this gene are a cause of long QT syndrome type 3 (LQT3), an autosomal dominant cardiac disease. Alternative splicing results in several transcript variants encoding different isoforms.

Gene names and symbols associated with SCN5A

  • sodium channel, voltage-gated, type V, alpha subunit (SCN5A) antibody
  • sodium channel, voltage-gated, type V, alpha (Scn5a) antibody
  • sodium channel, voltage-gated, type V, alpha subunit (Scn5a) antibody
  • CDCD2 antibody
  • CMD1E antibody
  • CMPD2 antibody
  • HB1 antibody
  • HB2 antibody
  • HBBD antibody
  • HH1 antibody
  • ICCD antibody
  • IVF antibody
  • LQT3 antibody
  • mH1 antibody
  • Nav1.5 antibody
  • Nav1.5c antibody
  • PFHB1 antibody
  • SCAL antibody
  • SkM1 antibody
  • SkM2 antibody
  • SSS1 antibody
  • VF1 antibody

Protein level used designations for SCN5A

sodium channel, voltage-gated, type V, alpha subunit , voltage-gated sodium channel type V alpha , sodium channel protein type 5 subunit alpha , voltage-gated sodium channel cardiac isoform Nav1.5 , sodium channel protein cardiac muscle subunit alpha , sodium channel protein type V subunit alpha , sodium channel voltage-gated type V alpha polypeptide , sodium channel, voltage-gated, type V, alpha polypeptide , voltage-gated sodium channel subunit alpha Nav1.5 , cardiac tetrodotoxin-insensitive voltage-dependent sodium channel alpha subunit , cardiac sodium channel , sodium channel alpha subunit , sodium channel, voltage-gated, type V, alpha (long QT syndrome 3) , voltage-gated sodium channel alpha subunit , sodium channel, voltage-gated, type V, alpha polypeptide (long (electrocardiographic) QT syndrome 3) , sodium channel, voltage-gated, type 5, alpha subunit , voltage-gated sodium channel Nav1.5c , oltage-gated sodium channel type V alpha , voltage-dependent sodium channel SCN10A , voltage-gated sodium channel H , voltage-gated sodium channel type V alpha polypeptide

GENE ID SPECIES
747523 Pan troglodytes
100034027 Equus caballus
20271 Mus musculus
6331 Homo sapiens
403497 Canis lupus familiaris
282061 Bos taurus
25665 Rattus norvegicus
395947 Gallus gallus
100009516 Oryctolagus cuniculus
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