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Merck

S0819

Sigma-Aldrich

Anti-Sodium Channel NaV1.5 antibody produced in rabbit

affinity isolated antibody, lyophilized powder

Synonym(e):

Anti-SKM2, Anti-Scn5a

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About This Item

MDL-Nummer:
UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

rabbit

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Form

lyophilized powder

Speziesreaktivität

rat

Methode(n)

western blot: 1:200 using rat heart membranes

UniProt-Hinterlegungsnummer

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

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

Verwandte Kategorien

Allgemeine Beschreibung

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).

Anwendung

Anti-Sodium Channel NaV1.5 antibody produced in rabbit has been in immunoblotting and immunofluorescence.

Biochem./physiol. Wirkung

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.

Physikalische Form

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

Haftungsausschluss

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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Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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Die Dokumentenbibliothek aufrufen

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.
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)
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
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
Hiroki Takanari et al.
Cardiovascular research, 111(4), 410-421 (2016-07-01)
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

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