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

The protein encoded by SCN5A is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. 再加上,我们可以发Sodium Channel, Voltage-Gated, Type V, alpha Subunit 抗体 (109)Sodium Channel, Voltage-Gated, Type V, alpha Subunit 蛋白 (11)和数多这个蛋白质的别的产品。

list all ELISA KIts 基因 基因ID UniProt
小鼠 SCN5A SCN5A 20271 Q9JJV9
 SCN5A SCN5A 6331 Q14524
大鼠 SCN5A SCN5A 25665 P15389

适于 Sodium Channel, Voltage-Gated, Type V, alpha Subunit 相互作用对的更多 ELISA 试剂盒

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

  1. identified two novel native phosphorylation sites in the C terminus of NaV1.5 that impair FGF13 (显示 FGF13 ELISA试剂盒)-dependent regulation of channel inactivation and may contribute to CaMKIIdeltac-dependent arrhythmogenic disorders in failing hearts.

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

  3. Loss of the C-terminus of connexin43 (显示 GJA1 ELISA试剂盒) limits microtubule plus-end capture and NaV1.5 localization at the intercalated disc.

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

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

  6. 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

  7. FoxO1 (显示 FOXO1 ELISA试剂盒) is involved in the modulation of NaV1.5 expression in ischemic heart disease.

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

  9. 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.

  10. Expression of NaV1.5 in cardiomyocytes is regulated by the PDZ domain (显示 INADL ELISA试剂盒)-binding motif.

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

  1. identified two novel native phosphorylation sites in the C terminus of NaV1.5 that impair FGF13 (显示 FGF13 ELISA试剂盒)-dependent regulation of channel inactivation and may contribute to CaMKIIdeltac-dependent arrhythmogenic disorders in failing hearts.

  2. Pathogenic variants in the SCN5A gene modify electrical excitability of sodium cannel that causes an imbalance in the currents of the different ions involved in the contraction process of the cardiomyocytes and induce ventricular remodeling and Dilated cardiomyopathy.

  3. Almost 2% of ARVD (显示 TGFB3 ELISA试剂盒)/C patients harbour rare SCN5A variants. For one of these variants, we demonstrated reduced sodium current, Nav1.5 and N-Cadherin (显示 CDH2 ELISA试剂盒) clusters at junctional sites. This suggests that Nav1.5 is in a functional complex with adhesion molecules, and reveals potential non-canonical mechanisms by which Nav1.5 dysfunction causes cardiomyopathy.

  4. The SCN5A variants R568H and A993T can be classified as pathogenic LQTS3 causing mutations.

  5. Brugada syndrome patients with SCN5A mutations exhibit more conduction abnormalities on ECG.

  6. One common intronic variant in SCN5A is linked with risk of Ventricular Fibrillation caused by first ST-Segment Elevation Myocardial Infarction.

  7. Nav1.5 is hyperacetylated on K1479 in the hearts of patients with cardiomyopathy and clinical conduction disease.

  8. BIMU8 is a potent blocker of hERG (显示 KCNH2 ELISA试剂盒), NaV1.5 and CaV1.2 (显示 CACNA1C ELISA试剂盒) cardiac ion channels, inducing cardiac arrhythmias.

  9. It might be important to suspect the coexistence of DCM and LQT3 (which is rare according to previous articles) in cases with this novel SCN5A missense mutation

  10. Mutational analysis across all 29 exons in SCN5A of the proband and first-degree relatives of the family revealed that the proband inherited a compound heterozygote mutation in SCN5A, specifically p.A226V and p.R1629X from each parent. The study is the first to report a SCN5A compound heterozygote in a Singaporean Chinese family.

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) 抗原简介

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

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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