• Product name
    Anti-Nav1.5/SCN5A antibody
    See all Nav1.5/SCN5A primary antibodies
  • Description
    Rabbit polyclonal to Nav1.5/SCN5A
  • Host species
  • Tested applications
    Suitable for: WB, IHC-P, ICC/IFmore details
  • Species reactivity
    Reacts with: Mouse, Human
    Predicted to work with: Rat, Rabbit, Horse, Chicken, Guinea pig, Cow, Cat, Dog, Chimpanzee, Zebrafish
  • Immunogen

    Synthetic peptide corresponding to Human Nav1.5/SCN5A aa 1857-1906.


  • Positive control
    • SW620 cell lysate and Human skin tissue.



Our Abpromise guarantee covers the use of ab56240 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB Use a concentration of 0.25 µg/ml. Detects a band of approximately 168 kDa (predicted molecular weight: 227 kDa). Good results were obtained when blocked with 5% non-fat dry milk in 0.05% PBS-T.
IHC-P Use a concentration of 4 - 8 µg/ml.
ICC/IF Use at an assay dependent concentration. PubMed: 20651255


  • Function
    This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-resistant Na(+) channel isoform. This channel is responsible for the initial upstroke of the action potential.
  • Tissue specificity
    Found in jejunal circular smooth muscle cells (at protein level). Expressed in human atrial and ventricular cardiac muscle but not in adult skeletal muscle, brain, myometrium, liver, or spleen. Isoform 4 is expressed in brain.
  • Involvement in disease
    Defects in SCN5A are a cause of progressive familial heart block type 1A (PFHB1A) [MIM:113900]; also known as Lenegre-Lev disease or progressive cardiac conduction defect (PCCD). PFHB1A is an autosomal dominant cardiac bundle branch disorder that may progress to complete heart block. PFHB1A is characterized by progressive alteration of cardiac conduction through the His-Purkinje system with right or left bundle branch block and widening of QRS complexes, leading to complete atrio-ventricular block and causing syncope and sudden death.
    Defects in SCN5A are the cause of long QT syndrome type 3 (LQT3) [MIM:603830]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. LQT3 inheritance is an autosomal dominant.
    Defects in SCN5A are the cause of Brugada syndrome type 1 (BRS1) [MIM:601144]. BRS1 is an autosomal dominant tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram (ECG). It can cause the ventricles to beat so fast that the blood is prevented from circulating efficiently in the body. When this situation occurs (called ventricular fibrillation), the individual will faint and may die in a few minutes if the heart is not reset.
    Defects in SCN5A are the cause of sick sinus syndrome type 1 (SSS1) [MIM:608567]. The term 'sick sinus syndrome' encompasses a variety of conditions caused by sinus node dysfunction. The most common clinical manifestations are syncope, presyncope, dizziness, and fatigue. Electrocardiogram typically shows sinus bradycardia, sinus arrest, and/or sinoatrial block. Episodes of atrial tachycardias coexisting with sinus bradycardia ('tachycardia-bradycardia syndrome') are also common in this disorder. SSS occurs most often in the elderly associated with underlying heart disease or previous cardiac surgery, but can also occur in the fetus, infant, or child without heart disease or other contributing factors, in which case it is considered to be a congenital disorder.
    Defects in SCN5A are the cause of ventricular fibrillation paroxysmal familial type 1 (VF1) [MIM:603829]. A cardiac arrhythmia marked by fibrillary contractions of the ventricular muscle due to rapid repetitive excitation of myocardial fibers without coordinated contraction of the ventricle and by absence of atrial activity.
    Defects in SCN5A can be a cause of sudden infant death syndrome (SIDS) [MIM:272120]. SIDS is the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of clinical history. Pathophysiologic mechanisms for SIDS may include respiratory dysfunction, cardiac dysrhythmias, cardiorespiratory instability, and inborn errors of metabolism, but definitive pathogenic mechanisms precipitating an infant sudden death remain elusive. Long QT syndromes-associated mutations can be responsible for some of SIDS cases.
    Defects in SCN5A may be a cause of familial atrial standstill (FAS) [MIM:108770]. Atrial standstill is an extremely rare arrhythmia, characterized by the absence of electrical and mechanical activity in the atria. Electrocardiographically, it is characterized by bradycardia, the absence of P waves, and a junctional narrow complex escape rhythm.
    Defects in SCN5A are the cause of cardiomyopathy dilated type 1E (CMD1E) [MIM:601154]; also known as dilated cardiomyopathy with conduction disorder and arrhythmia or dilated cardiomyopathy with conduction defect 2. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
  • Sequence similarities
    Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.5/SCN5A subfamily.
    Contains 1 IQ domain.
  • Domain
    The sequence contains 4 internal repeats, each with 5 hydrophobic segments (S1,S2,S3,S5,S6) and one positively charged segment (S4). Segments S4 are probably the voltage-sensors and are characterized by a series of positively charged amino acids at every third position.
  • Post-translational
    Ubiquitinated by NEDD4L; which promotes its endocytosis. Does not seem to be ubiquitinated by NEDD4 or WWP2.
  • Cellular localization
  • Information by UniProt
  • Database links
  • Alternative names
    • Cardiac tetrodotoxin insensitive voltage dependent sodium channel alpha subunit antibody
    • CDCD2 antibody
    • CMD1E antibody
    • CMPD2 antibody
    • HB1 antibody
    • HB2 antibody
    • HBBD antibody
    • HH1 antibody
    • ICCD antibody
    • IVF antibody
    • LQT3 antibody
    • PFHB1 antibody
    • Scn5a (gene name) antibody
    • Scn5a antibody
    • SCN5A_HUMAN antibody
    • Sodium channel protein cardiac muscle alpha subunit antibody
    • Sodium channel protein cardiac muscle subunit alpha antibody
    • Sodium channel protein type 5 subunit alpha antibody
    • Sodium channel protein type V alpha subunit antibody
    • Sodium channel protein type V subunit alpha antibody
    • SSS1 antibody
    • VF1 antibody
    • Voltage gated sodium channel alpha subunit Nav1.5 antibody
    • Voltage-gated sodium channel subunit alpha Nav1.5 antibody
    see all


  • Anti-Nav1.5/SCN5A antibody (ab56240) at 0.25 µg/ml + SW620 cell lysate at 10 µg

    HRP conjugated anti-Rabbit IgG at 1/50000 dilution

    Predicted band size: 227 kDa
    Observed band size: 168 kDa
    why is the actual band size different from the predicted?

    Gel concentration: 8%
  • ab56240 (4µg/ml) staining Human Nav1.5/SCN5A in skin tissue by immunohistochemistry on paraffin embedded tissue. The arrows indicate positively stained squamous epithelial cells. Magnification 400X.


This product has been referenced in:
  • Hendrickse P  et al. An evaluation of common markers of muscle denervation in denervated young-adult and old rat gastrocnemius muscle. Exp Gerontol 106:159-164 (2018). IHC-P ; Human . Read more (PubMed: 29524469) »
  • Wei XH  et al. Inhibition of late sodium current suppresses calcium-related ventricular arrhythmias by reducing the phosphorylation of CaMK-II and sodium channel expressions. Sci Rep 7:981 (2017). WB ; Rabbit . Read more (PubMed: 28428622) »
See all 10 Publications for this product

Customer reviews and Q&As

Abcam has not validated the combination of species/application used in this Abreview.
Western blot
Rabbit Tissue lysate - other (heart)
Gel Running Conditions
Reduced Denaturing (8%)
Loading amount
50 µg
Blocking step
BSA as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 3% · Temperature: 25°C

Miss. Dai-Er Li

Verified customer

Submitted Jul 11 2017


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