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SCN5A Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q14524 |
| Other Accession | P15389, Q9JJV9, NP_000326.2 |
| Reactivity | Human |
| Predicted | Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 226940 Da |
| Antigen Region | 42-70 aa |
| Gene ID | 6331 |
|---|---|
| Other Names | 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 |
| Target/Specificity | This SCN5A antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 42-70 amino acids from the N-terminal region of human SCN5A. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | SCN5A Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | SCN5A (HGNC:10593) |
|---|---|
| Function | Pore-forming subunit of Nav1.5, a voltage-gated sodium (Nav) channel that directly mediates the depolarizing phase of action potentials in excitable membranes. Navs, also called VGSCs (voltage- gated sodium channels) or VDSCs (voltage-dependent sodium channels), operate by switching between closed and open conformations depending on the voltage difference across the membrane. In the open conformation they allow Na(+) ions to selectively pass through the pore, along their electrochemical gradient. The influx of Na(+) ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues (PubMed:1309946, PubMed:21447824, PubMed:23085483, PubMed:23420830, PubMed:25370050, PubMed:26279430, PubMed:26392562, PubMed:26776555). Nav1.5 is the predominant sodium channel expressed in myocardial cells and it is responsible for the initial upstroke of the action potential in cardiac myocytes, thereby initiating the heartbeat (PubMed:11234013, PubMed:11804990, PubMed:12569159, PubMed:1309946). Required for normal electrical conduction including formation of the infranodal ventricular conduction system and normal action potential configuration, as a result of its interaction with XIRP2 (By similarity). |
| Cellular Location | Cell membrane; Multi-pass membrane protein {ECO:0000250|UniProtKB:P15389}. Cytoplasm, perinuclear region. Cell membrane, sarcolemma, T- tubule {ECO:0000250|UniProtKB:P15389}. Cell junction {ECO:0000250|UniProtKB:P15389}. Note=RANGRF promotes trafficking to the cell membrane. Colocalizes with PKP2 at intercalated disks in the heart (By similarity). {ECO:0000250|UniProtKB:P15389, ECO:0000269|PubMed:21447824, ECO:0000269|PubMed:23420830} |
| Tissue Location | Found in jejunal circular smooth muscle cells (at protein level). Expressed in human atrial and ventricular cardiac muscle but not in adult skeletal muscle, brain, myometrium, liver, or spleen. Isoform 4 is expressed in brain. |
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
Liu, M., et al. Circ. Res. 107(8):967-974(2010)
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
van Stuijvenberg, L., et al. DNA Cell Biol. 29(10):577-587(2010)
House, C.D., et al. Cancer Res. 70(17):6957-6967(2010)
Garcia-Castro, M., et al. Rev Esp Cardiol 63(7):856-859(2010)
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