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

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 many more products for this protein.

list all proteins Gene Name GeneID UniProt
SCN5A 20271 Q9JJV9
SCN5A 6331 Q14524
Rat SCN5A SCN5A 25665 P15389
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Top Sodium Channel, Voltage-Gated, Type V, alpha Subunit Proteins at antibodies-online.com

Showing 5 out of 11 products:

Catalog No. Origin Source Conjugate Images Quantity Supplier Delivery Price Details
HOST_Escherichia coli (E. coli) Mouse His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 29 to 34 Days
$4,331.68
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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 29 to 34 Days
$4,331.68
Details
Insect Cells Mouse His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 49 Days
$5,442.50
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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 49 Days
$5,442.50
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HOST_Wheat germ Human GST tag 10 μg Log in to see 9 Days
$405.71
Details

SCN5A Proteins by Origin and Source

Origin Expressed in Conjugate
Mouse (Murine) ,

Human , ,
,

More Proteins for Sodium Channel, Voltage-Gated, Type V, alpha Subunit (SCN5A) 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 Proteins) limits microtubule plus-end capture and NaV1.5 localization at the intercalated disc.

  3. Ser571-mediated increases in INa (show INA Proteins),L promote abnormal repolarization and intracellular Ca(2 (show CA2 Proteins)+) 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 Proteins)+) contributes to the regulation of INaL conducted by NaV1.5 mutants and propose that, during excitation-contraction coupling, elevated intracellular Ca(2 (show CA2 Proteins)+) 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 Proteins) 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-binding motif.

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

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

  1. These results suggested that neferine can block Nav1.5 channels under the open state and inactivating state and it is an open channel blocker of Nav1.5 channels.

  2. Molecular and pharmacological characterization of the SCN5A p.I141V mutation provide new evidence supporting the association of this mutation with exercise-induced polymorphic ventricular arrhythmias. These data also demonstrate that flecainide may serve as an effective treatment for the defect in Nav 1.5 that leads to an increased sodium window current.

  3. 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.

  4. 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.

  5. 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

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

  7. 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.

  8. 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 Proteins) (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

  9. 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.

  10. Identifies alphaB-crystallin (show CRYAB Proteins) as a new binding partner for Nav1.5. alphaB-Crystallin (show CRYAB Proteins) interacts with Nav1.5 and increases INa (show INA Proteins) 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 (show CRYAB Proteins) and Nav1.5 and between alphaB-crystallin (show CRYAB Proteins) and functionally active Nedd4-2 (show NEDD4L Proteins).

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) Protein Profile

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

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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