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

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 Proteins (11) and and many more products for this protein.

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

Showing 10 out of 97 products:

Catalog No. Reactivity Host Conjugate Application Images Quantity Supplier Delivery Price Details
Cow Rabbit Un-conjugated IHC, WB WB Suggested Anti-SCN5A Antibody Titration: 0.2-1 ug/mlELISA Titer: 1:12500Positive Control: Human Muscle WB Suggested Anti-SCN5A Antibody Titration:  0.2-1 ug/ml  ELISA Titer:  1:12500  Positive Control:  Human Muscle 100 μL Log in to see 2 to 3 Days
$319.00
Details
Cow Rabbit Un-conjugated WB WB Suggested Anti-SCN5A Antibody Titration:  0.2-1 ug/ml  ELISA Titer:  1:312500  Positive Control:  SW620 cell lysate SCN5A is supported by BioGPS gene expression data to be expressed in SW620 Host:  Rabbit  Target Name:  SCN5A  Sample Type:  MCF7 Whole Cell  Lane A:  Primary Antibody  Lane B:  Primary Antibody + Blocking Peptide  Primary Antibody Concentration:  1ug/ml  Peptide Concentration:  5ug/ml  Lysate Quantity:  25ug/lane/Lane  Gel Concentration:  0.12 100 μL Log in to see 2 to 3 Days
$319.00
Details
Cow Rabbit Un-conjugated IHC, WB Rabbit Anti-SCN5A Antibody  Catalog Number: ARP34935_P050 Formalin Fixed Paraffin Embedded Tissue: Human Adult heart  Observed Staining: Membrane (stronger than with ARP34934) Primary Antibody Concentration: 1:600 Secondary Antibody: Donkey anti-Rabbit-Cy2/3 Secondary Antibody Concentration: 1:200 Magnification: 20X Exposure Time: 0.5 – 2.0 sec Protocol located in Reviews and Data. WB Suggested Anti-SCN5A Antibody Titration: HEK cel lysate; HEK cel with HuNav1.5 transfected lysate; Mouse Heart lysate80 ug protein on gelQC Antibodies 1:100 in PBS/Tweensecondary antibodie 1:10.000 ( IRDYE 800 CWGoat anti Rabbit IgG) analyse with the Licor Odyssey Positive Control: HEK cel lysate; HEK cel with HuNav1.5 transfected lysate; Mouse Heart lysate80 ug protein on gelQC Antibodies 1:100 in PBS/Tweensecondary antibodie 1:10.000 ( IRDYE 800 CWGoat anti Rabbit IgG) analyse with the Licor Odyssey 100 μL Log in to see 2 to 3 Days
$289.00
Details
Mouse Rabbit Un-conjugated WB Western blot analysis of Nav1.5 expression in mouse cardiac muscle extract ( Lane 1). Nav1.5 at 250KD was detected using rabbit anti-Nav1.5 Antigen Affinity purified polyclonal antibody (Catalog # ) at 0.5 ??g/mL. The blot was developed using chemiluminescence (ECL) method (Catalog # EK1002). 100 μg Log in to see 4 to 6 Days
$240.00
Details
Human Goat Un-conjugated ELISA   100 μg Log in to see 6 to 7 Days
$291.53
Details
Human Goat Un-conjugated ELISA, IHC   100 μg Log in to see 6 to 7 Days
$429.84
Details
Human Goat Un-conjugated ELISA, IHC, IHC (p) Human Brain, Cortex (formalin-fixed, paraffin-embedded) stained with SCN5A antibody ABIN290512 at 5-10 ug/ml followed by biotinylated anti-goat IgG secondary antibody ABIN481715, alkaline phosphatase-streptavidin and chromogen. Anti-SCN5A / Nav1.5 antibody IHC of human brain, cortex. Immunohistochemistry of formalin-fixed, paraffin-embedded tissue after heat-induced antigen retrieval. Antibody concentration 10 ug/ml. 50 μg Log in to see 11 to 14 Days
$484.00
Details
Dog Rabbit Un-conjugated IHC, IHC (p) Anti-SCN5A / Nav1.5 antibody  ABIN1049322 IHC staining of human heart. Immunohistochemistry of formalin-fixed, paraffin-embedded tissue after heat-induced antigen retrieval. Anti-SCN5A / Nav1.5 antibody IHC of human heart. Immunohistochemistry of formalin-fixed, paraffin-embedded tissue after heat-induced antigen retrieval. 50 μg Log in to see 11 to 14 Days
$484.00
Details
Bat Rabbit Un-conjugated WB 50 μg Log in to see 11 to 14 Days
$551.83
Details
Cow Goat Un-conjugated ELISA, IHC, IHC (p) Western Blot: Nav1.5 Antibody [ABIN269816] - Rat Brain lysate . Immunohistochemistry-Paraffin: Nav1.5 Antibody [ABIN269816] - Mouse Brain. 0.1 mg Log in to see 7 to 9 Days
$375.73
Details

Top referenced anti-Sodium Channel, Voltage-Gated, Type V, alpha Subunit Antibodies

  1. Cow (Bovine) Polyclonal SCN5A Primary Antibody for WB - ABIN2776347 : Shah, Wingo, Weiss, Williams, Balser, Chazin: Calcium-dependent regulation of the voltage-gated sodium channel hH1: intrinsic and extrinsic sensors use a common molecular switch. in Proceedings of the National Academy of Sciences of the United States of America 2006 (PubMed)
    Show all 5 Pubmed References

  2. Cow (Bovine) Polyclonal SCN5A Primary Antibody for ELISA, IHC - ABIN269816 : Olson, Michels, Ballew, Reyna, Karst, Herron, Horton, Rodeheffer, Anderson: Sodium channel mutations and susceptibility to heart failure and atrial fibrillation. in JAMA 2005 (PubMed)

  3. Cow (Bovine) Polyclonal SCN5A Primary Antibody for IHC, WB - ABIN2776088 : Van Norstrand, Tester, Ackerman: Overrepresentation of the proarrhythmic, sudden death predisposing sodium channel polymorphism S1103Y in a population-based cohort of African-American sudden infant death syndrome. in Heart rhythm : the official journal of the Heart Rhythm Society 2008 (PubMed)
    Show all 2 Pubmed References

More Antibodies against Sodium Channel, Voltage-Gated, Type V, alpha Subunit Interaction Partners

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

  1. Deletion of Nav1.5 from astrocytes leads to significantly worsened clinical outcomes in experimental autoimmune encephalomyelitis (EAE), with increased inflammatory infiltrate in both early and late stages of disease in a sex-specific manner. Removal of Nav1.5 in astrocytes leads to increased inflammation in female mice with EAE, including increased astroglial response and infiltration of T cells and phagocytic monocytes.

  2. The late sodium current inhibitor GS-458967 exhibits anti-arrhythmic potential in cardiac myocytes from Scn5a-1798insD+/- mice.

  3. Our findings indicate that H2O2 inhibits NaV1.5 expression by activating the Wnt/b-catenin signaling and beta-catenin interacts with TCF4 to transcriptionally suppress cardiac NaV1.5 expression.

  4. identified two novel native phosphorylation sites in the C terminus of NaV1.5 that impair FGF13-dependent regulation of channel inactivation and may contribute to CaMKIIdeltac-dependent arrhythmogenic disorders in failing hearts.

  5. Tetrodotoxin-sensitive alpha-subunits of voltage-gated sodium channels are relevant for inhibition of cardiac sodium currents by local anesthetics.

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

  7. Loss of the C-terminus of connexin43 limits microtubule plus-end capture and NaV1.5 localization at the intercalated disc.

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

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

  10. 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

  11. FoxO1 is involved in the modulation of NaV1.5 expression in ischemic heart disease.

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

  13. 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.

  14. Expression of NaV1.5 in cardiomyocytes is regulated by the PDZ domain-binding motif.

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

  16. Nav1.5 expression was reduced in both RyR2(S/S) and Scn5a(+/-) atria

  17. disruption of the molecular clock in the adult heart slows heart rate, increases arrhythmias, and decreases the functional expression of Scn5a.

  18. AP durations were smallest in the RV of Scn5a+/-, fulfilling predictions of an increased heterogeneity of repolarization as an additional possible electrophysiological mechanism for arrhythmogenesis in BrS.

  19. For Brugada syndrome mutation G1743R, MOG1 restored the impaired PM expression of the mutant protein and restored I(Na) in a heterozygous state (mixture of wild type and mutant Na(v)1.5) to a full level of a homozygous wild-type state.

  20. Stronger expressions of SCN5a, SCN1b and Kir2.1 were observed in ventricular-like and atrial-like cells compared to that of pacemaker-like cardiomyocytes.

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

  1. This also indicated that SCN5A(R1193Q) does not modulate the NaV1.5 channel in response to an acute body temperature change. Therefore, SCN5A(R1193Q) may not be a monogenic factor that triggers arrhythmic disorders.

  2. Gain- or loss-of-function mutations in different regions of the SCNA5 gene that cause arrhythmias can be classified according to their impact on inward-peak, or inward-late sodium currents in cardiomyocytes.

  3. Using the simple, non-invasive echocardiographic parameter RVED revealed a more pronounced 'electromechanical' delay in BrS patients carrying premature protein truncation variants of SCN5A, rather than missense variants.

  4. We identified SCN5A CNVs in 2.9% of BrS probands who were symptomatic or had a family history.

  5. Study shows that NaV1.5 channel is inactivated by CaM which binds two sites in the intracellular loop in a Ca-dependent manner.

  6. R222Q SCN5A mutation is associated with response to chemotherapy in Purkinje-related ventricular arrhythmia and familial dilated cardiomyopathy.

  7. association between familial dilated cardiomyopathy and the rs1805124 polymorphism in the SCN5A gene

  8. SCN5A mutation is associated with an increased risk of drug-induced ventricular arrhythmia.

  9. Reduced expression of HuR may be at least partially responsible for the downregulation of SCN5A mRNA expression in ischemic HF. Overexpression of HuR may rescue decreased SCN5A expression and reduce arrhythmic risk in HF

  10. We identified a genetic variant that is associated with local anesthetic resistance in the gene encoding for Nav1.5. We also demonstrate that Nav1.5 is present in human peripheral nerves to support the plausibility that an abnormal form of the Nav1.5 protein could be responsible for the observed local anesthetic resistance. Specifically, we noted the A572D mutation in the SCN5A gene encoding for Nav1.5.

  11. Results demonstrate a novel pleiotropic phenotype arising from the compound SCN5A mutation, P1332L and A647D. The lethal LQT3 phenotype of P1332L was mitigated with the Brugada- associated A647D, which negated the previously reported therapeutic benefit of mexiletine. Concurrently, the A647 mutant reduced Na current sufficiently to produce a novel global cardiac conduction defect affecting the atria and ventricles.

  12. Study data suggest that SAR1A and SAR1B are the critical regulators of trafficking of Nav1.5. Moreover, SAR1A and SAR1B interact with MOG1, and are required for MOG1-mediated cell surface expression and function of Nav1.5.

  13. The failing heart has ~30% lower SCN5A levels.

  14. novel variants in SCN5A, KCNH2 and KCNQ1 are associated with congenital long QT syndrome in a Polish population

  15. The results of this study obtained in a sample from the German population do not provide evidence for an involvement of the investigated gene polymorphisms as major susceptibility factors in the pathophysiology of QTc prolongation.

  16. Our study expands the spectrum of SCN5A mutations and contributes to genetic counselling of families with arrhythmia.

  17. Here the authors show that SGK1 directly regulates NaV1.5 channel function.

  18. The 1795insD mutation in SCN5A reduced the beating rate of the model cell from 74 to 69 beats/min.

  19. Using a human-induced pluripotent stem cells -based model forSCN5A-D1275N-related sodium channelopathy, it was demonstrated that diminished sodium currents resulting from lower NaV1.5 protein levels, which is dependent on proteasomal degradation.

  20. We identified a double heterozygosity for pathogenic mutations in SCN5A and TRPM4 in a Brugada syndrome patient.

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

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 voltage-gated channel alpha subunit 5 (SCN5A) antibody
  • sodium channel, voltage-gated, type V, alpha (Scn5a) antibody
  • sodium voltage-gated channel alpha subunit 5 (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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