mProX™ Human SCN5A Stable Cell Line

Product Information

Target Protein

SCN5A

Target Family

Voltage Gated Sodium Channel

Target Protein Species

Human

Host Cell Type

MCF-7; CHO-K1; HEK293

Target Classification

Ion Channel Cell Lines

Target Research Area

Cardiovascular Research; CNS Research

Related Diseases

Sudden Infant Death Syndrome; Long Qt Syndrome

Gene ID

6331

UniProt ID

Q14524

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

The major cardiac sodium channel Nav1.5's alpha subunit, which is believed to be in charge of preserving INa's proper operation, is encoded by the SCN5A gene. The key element of the quick depolarization phase is INa current, which is followed by the excitation-contraction coupling cascade and the correct conduction of the electrical impulse in the heart. Numerous inherited cardiac channelopathies, such as Brugada syndrome, long QT syndrome, and malfunction of the cardiac conduction system, are caused by genetic variations in SCN5A. SCN5A mutations have also been linked to heart failure, dilated cardiomyopathy, and myocardial contractile dysfunction. The primary pathogenic mechanisms behind sodium channelopathies caused by SCN5A variants have been clarified by research using the patch clamp technique and transgenic animal technologies. The customized SCN5A stable cell line can be used in antibody discovery and development, potential drug candidate screening and signaling pathway researches.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Patricia (Verified Customer)

Is there a link between the SCN5A gene and opioid use disorder? Jun 25 2020

chat Sherry Smith (Creative Biolabs Scientific Support)

Yes, hypermethylation in the promoter region of the SCN5A gene has been associated with opioid use disorder. Jun 25 2020

chat Brian (Verified Customer)

How does SCN5A relate to schizophrenia in the Chinese population? Dec 06 2022

chat Sherry Smith (Creative Biolabs Scientific Support)

Variants in the promoter of the SCN5A gene do not seem to play a major role in susceptibility to schizophrenia in the Chinese population. Dec 06 2022

Published Data

Fig.1 SCN5A/NaV1.5 in MCF-7 cells.

In moderately aggressive MCF-7 cells, SCN5A/NaV1.5 heterologous expression promotes the invasive phenotype. Typical images of NaV1.5-GFP transfected MCF-7 cells in phase contrast (left) and in epifluorescence (right), 24 hours after transfection.

Ref: Gradek, Frédéric, et al. "Sodium channel Na v 1.5 controls epithelial-to-mesenchymal transition and invasiveness in breast cancer cells through its regulation by the salt-inducible kinase-1." Scientific reports 9.1 (2019): 18652.

Pubmed: 31819138

DOI: 10.1038/s41598-019-55197-5

Research Highlights

Zaklyazminskaya, Elena, and Sergei Dzemeshkevich. "The role of mutations in the SCN5A gene in cardiomyopathies." Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1863.7 (2016): 1799-1805.
Pubmed: 26916278 DOI: 10.1016/j.bbamcr.2016.02.014

Clinicians can now develop mutation-specific diagnostic and treatment plans for patients with SCN5A mutations, as well as gene-specific risk stratification schemes, thanks to growing understanding of the function of SCN5A in health and disease.
Wilde, Arthur AM, and Ahmad S. Amin. "Clinical spectrum of SCN5A mutations: long QT syndrome, Brugada syndrome, and cardiomyopathy." JACC: Clinical Electrophysiology 4.5 (2018): 569-579.
Pubmed: 29798782 DOI: 10.1016/j.jacep.2018.03.006