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Key Documents

S0819

Sigma-Aldrich

Anti-Sodium Channel NaV1.5 antibody produced in rabbit

affinity isolated antibody, lyophilized powder

Synonyme(s) :

Anti-SKM2, Anti-Scn5a

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

lyophilized powder

Espèces réactives

rat

Technique(s)

western blot: 1:200 using rat heart membranes

Numéro d'accès UniProt

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SCN5A(6331)
mouse ... Scn5a(20271)
rat ... Scn5a(25665)

Description générale

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.

Immunogène

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.

Actions biochimiques/physiologiques

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.

Forme physique

Lyophilized at ~0.8 mg/mL in phosphate buffered, pH 7.4, containing 1% bovine serum albumin, and 0.05% sodium azide.

Clause de non-responsabilité

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.

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Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Exome Sequencing Identifies Compound Heterozygous Mutations in SCN5A Associated with Congenital Complete Heart Block in the Thai Population
Thongnak C, et al.
Disease Markers (2016)
Liang Guo et al.
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.
Joyce C K Man et al.
Nature communications, 10(1), 4943-4943 (2019-11-02)
Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia disorders. Here, we identify an evolutionary conserved regulatory cluster with super enhancer characteristics downstream of
Ivan Gando et al.
Forensic science international, 301, 289-298 (2019-06-14)
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
Jérôme Clatot et al.
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

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