Sodium channel protein type 5 subunit alpha; HH1; Sodium channel protein cardiac muscle subunit alpha; Sodium channel protein type V subunit alpha; Voltage-gated sodium channel subunit alpha Nav15; SCN5A

For Research Use Only. Not for use in diagnostic procedures.

Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.

Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C.

Small volumes of SCN5A blocking peptide vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-resistant Na(+) channel isoform. This channel is responsible for the initial upstroke of the action potential. Channel inactivation is regulated by intracellular calcium levels.

224,917 Da

sodium voltage-gated channel alpha subunit 5

sodium channel protein type 5 subunit alpha

Sodium channel protein type 5 subunit alpha

SCN5A_HUMAN

The protein encoded by this gene is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. This protein is found primarily in cardiac muscle and is responsible for the initial upstroke of the action potential in an electrocardiogram. Defects in this gene are a cause of long QT syndrome type 3 (LQT3), an autosomal dominant cardiac disease. Alternative splicing results in several transcript variants encoding different isoforms. [provided by RefSeq, Jul 2008]

SCN5A: an integral membrane protein and a voltage-gated sodium channel subunit. Mediates the voltage-dependent sodium ion permeability of excitable membranes. This protein is found primarily in cardiac muscle and is responsible for the initial upstroke of the action potential in an electrocardiogram. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-resistant Na(+) channel isoform. Intracellular calcium levels regulate channel inactivation. Interacts with the PDZ domain of the syntrophin SNTA1, SNTB1 and SNTB2. Interacts with NEDD4, NEDD4L, WWP2 and GPD1L. Defects in this protein are a cause of long QT syndrome type 3 (LQT3). Belongs to the sodium channel (TC 1.A.1.10) family, Nav1.5/SCN5A subfamily. 6 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, multi-pass; Channel, sodium; Membrane protein, integral

Chromosomal Location of Human Ortholog: 3p21

Cellular Component: caveola; cell surface; endoplasmic reticulum; integral to membrane; intracellular; lateral plasma membrane; plasma membrane; sarcolemma; T-tubule; voltage-gated sodium channel complex; Z disc

Molecular Function: ankyrin binding; calmodulin binding; enzyme binding; fibroblast growth factor binding; nitric-oxide synthase binding; protein binding; protein domain specific binding; protein kinase binding; ubiquitin protein ligase binding; voltage-gated sodium channel activity

Biological Process: cardiac muscle contraction; cerebellum development; generation of action potential; membrane depolarization; odontogenesis of dentine-containing teeth; positive regulation of action potential; positive regulation of epithelial cell proliferation; regulation of heart rate; response to denervation involved in regulation of muscle adaptation; sodium ion transport; telencephalon development

Disease: Atrial Fibrillation, Familial, 10; Brugada Syndrome 1; Cardiomyopathy, Dilated, 1e; Long Qt Syndrome 3; Progressive Familial Heart Block, Type Ia; Sick Sinus Syndrome 1, Autosomal Recessive; Sudden Infant Death Syndrome; Ventricular Fibrillation During Myocardial Infarction, Susceptibility To

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