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SCN5A / Nav1.5 Antibody (Internal)
Goat Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, E |
|---|---|
| Primary Accession | Q14524 |
| Reactivity | Human |
| Host | Goat |
| Clonality | Polyclonal |
| Calculated MW | 227kDa |
| Dilution | ELISA (1:32000), IHC-P (5-10 µg/ml), |
| 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 Nav1.5, SCN5A |
| Target/Specificity | Human SCN5A / Nav1.5. This antibody is expected to recognise all reported isoforms (NP_932173.1; NP_000326.2; NP_001092874.1; NP_001092875.1). |
| Reconstitution & Storage | Store at -20°C. Minimize freezing and thawing. |
| Precautions | SCN5A / Nav1.5 Antibody (Internal) 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. |
| Volume | 50 µl |
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
Gellens M.E.,et al.Proc. Natl. Acad. Sci. U.S.A. 89:554-558(1992).
Ou Y.,et al.Neurogastroenterol. Motil. 14:477-486(2002).
Makielski J.C.,et al.Circ. Res. 93:821-828(2003).
Ye B.,et al.Physiol. Genomics 12:187-193(2003).
Ou S.-W.,et al.Eur. J. Neurosci. 22:793-801(2005).
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