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. Zusätzlich bieten wir Ihnen Sodium Channel, Voltage-Gated, Type V, alpha Subunit Antikörper (109) und Sodium Channel, Voltage-Gated, Type V, alpha Subunit Proteine (11) und viele weitere Produktgruppen zu diesem Protein an.

list all ELISA KIts Gen GeneID UniProt
Anti-Maus SCN5A SCN5A 20271 Q9JJV9
Anti-Human SCN5A SCN5A 6331 Q14524
Anti-Ratte SCN5A SCN5A 25665 P15389
Direkt bei antikoerper-online bestellen
  • +49 (0)241 95 163 153
  • +49 (0)241 95 163 155
  • Online bestellen
  • orders@antikoerper-online.de

Weitere ELISA Kits für Sodium Channel, Voltage-Gated, Type V, alpha Subunit Interaktionspartner

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

  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 (zeige GJA1 ELISA Kits) limits microtubule plus-end capture and NaV1.5 localization at the intercalated disc.

  3. Ser571-mediated increases in INa (zeige INA ELISA Kits),L promote abnormal repolarization and intracellular Ca(2 (zeige 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 (zeige 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 (zeige 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 (zeige 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 (zeige INADL ELISA Kits)-binding motif.

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

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

  1. Almost 2% of ARVD (zeige TGFB3 ELISA Kits)/C patients harbour rare SCN5A variants. For one of these variants, we demonstrated reduced sodium current, Nav1.5 and N-Cadherin (zeige CDH2 ELISA Kits) 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.

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

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

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

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

  6. BIMU8 is a potent blocker of hERG (zeige KCNH2 ELISA Kits), NaV1.5 and CaV1.2 (zeige CACNA1C ELISA Kits) cardiac ion channels, inducing cardiac arrhythmias.

  7. 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

  8. 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.

  9. Clinically relevant cardiotoxicity of domperidone and metoclopramide corresponds to a rather potent and local anesthetic-like inhibition of cardiac Na channels including Nav1.5.

  10. The H558R polymorphism in the SCN5A gene has been associated with the LQT3 syndrome and possibly can influence repolarization and depolarization of cardiac muscle cells.

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

  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-Profil

Beschreibung des Gens

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.

Genbezeichner und Symbole assoziert mit SCN5A

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

Bezeichner auf Proteinebene für 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 SPEZIES
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
Haben Sie etwas anderes gesucht?