SCN5A (sodium voltage-gated channel α subunit 5) codes for an α subunit of the cardiac sodium channel (NaV1.5). It is located on human chromosome 3p22.2.
Immunogen
peptide corresponding to amino acid residues 493-511 of rH1 (Accession P15389). This epitope is identical in mouse and highly homologous in human (17/19 residues identical).
Application
Anti-Sodium Channel NaV1.5 antibody produced in rabbit has been in immunoblotting and immunofluorescence.[1]
Biochem/physiol Actions
SCN5A (sodium voltage-gated channel α subunit 5) regulates the movement of sodium ions into cells, which helps in the production and diffusion of electrical impulses. SCN5A mutations results in the loss or gain of sodium channel activity and cause several cardiac diseases like Brugada syndrome, Long QT syndrome type 3, Sick sinus syndrome and progressive familial heart block.
Physical form
Lyophilized at ~0.8 mg/mL in phosphate buffered, pH 7.4, containing 1% bovine serum albumin, and 0.05% sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Multiple genome-wide association studies (GWAS) and targeted gene sequencing have identified common variants in SCN10A in cases of PR and QRS duration abnormalities, atrial fibrillation and Brugada syndrome. The New York City Office of Chief Medical Examiner has now also
American journal of physiology. Heart and circulatory physiology, 315(5), H1250-H1257 (2018-08-18)
Mutations in voltage-gated Na+ channels have been linked to several channelopathies leading to a wide variety of diseases including cardiac arrhythmias, epilepsy, and myotonia. We have previously demonstrated that voltage-gated Na+ channel (Nav)1.5 trafficking-deficient mutant channels could lead to a
In healthy hearts, ventricular gap junctions are mainly composed by connexin43 (Cx43) and localize in the intercalated disc, enabling appropriate electrical coupling. In diseased hearts, Cx43 is heterogeneously down-regulated, whereas activity of calmodulin/calcium-calmodulin protein kinase II (CaM/CaMKII) signalling increases. It
Exome Sequencing Identifies Compound Heterozygous Mutations in SCN5A Associated with Congenital Complete Heart Block in the Thai Population
Toxicological sciences : an official journal of the Society of Toxicology, 123(1), 281-289 (2011-06-23)
Improved in vitro systems for predicting drug-induced toxicity are needed in the pharmaceutical and biotechnology industries to decrease late-stage drug attrition. One unmet need is an early screen for cardiotoxicity, which accounts for about one third of safety-based withdrawn pharmaceuticals.
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.