S0819
Anti-Sodium Channel NaV1.5 antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Sinónimos:
Anti-SKM2, Anti-Scn5a
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About This Item
Productos recomendados
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
rat
technique(s)
western blot: 1:200 using rat heart membranes
UniProt accession no.
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... SCN5A(6331)
mouse ... Scn5a(20271)
rat ... Scn5a(25665)
General description
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.
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.
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Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificados de análisis (COA)
Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»
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Encuentre la documentación para los productos que ha comprado recientemente en la Biblioteca de documentos.
María Gallego-Delgado et al.
International journal of molecular sciences, 25(9) (2024-05-11)
A novel rare mutation in the pore region of Nav1.5 channels (p.L889V) has been found in three unrelated Spanish families that produces quite diverse phenotypic manifestations (Brugada syndrome, conduction disease, dilated cardiomyopathy, sinus node dysfunction, etc.) with variable penetrance among
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
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