|Application ||WB, IP|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||221387 Da|
|Homology||Mouse - 12/14 amino acid residues identical.|
|Other Names||Sodium channel protein type 3 subunit alpha, Sodium channel protein brain III subunit alpha, Sodium channel protein type III subunit alpha, Voltage-gated sodium channel subtype III, Voltage-gated sodium channel subunit alpha Nav13, Scn3a|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide (C)HLEGNHRADGDRFP, corresponding to amino acid residues 511-524 rat Nav1.3 (Accession P08104).ֲ ֲ Intracellular, loop between domains I and II.|
|Peptide Confirmation||Confirmed by amino acid analysis.|
|Application Details||Western blot analysis (WB): - Mouse brain (see Verret, L. et al. (2012) in Product Citations). - Mouse brain membrane lysate (see Kim, D.Y. et al. (2011) in Product Citations). Immunoprecipitation (IP): - CNahIII-12 cells expressing human NaV1.3 and β1 subunit. (see Meadows, L.S. et al. (2002) in Product Citations). Immunohistochemistry (IH): - Rat brain sections (1:250) (see Hargus, N.J. et al. (2013) in Product Citations). - Rat brain sections (1:200) (see Lindia, J.A. and Abbadie, C. (2003) in Product Citations). Immunocytochemistry (IC): - Mouse LVA myocytes (1:100) (see Ednie, A.R. et al. (2013) in Product Citations).|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||1 mg/ml.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 µl water.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||0.75 µg peptide per 1 µg antibody.|
|Formulation||Lyophilized powder. Reconstituted antibody contains phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.05% NaN3.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Voltage-gated sodium channels (Nav) are essential for the generation of action potentials and for cell excitability.1 Nav channels are activated in response to depolarization and selectively allow flow of Na+ ions. To date, nine Nav α subunits have been cloned and named Nav1.1-Nav1.9.4-5 The Nav channels are classified into two groups according to their sensitivity to Tetrodotoxin (TTX): TTX-sensitive (Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6 and Nav1.7) and TTX-resistant (Nav1.5, Nav1.8 and Nav1.9).2-3 Mammalian sodium channels are heterotrimers, composed of a central, pore-forming α subunit and two auxiliary β subunits. The expression of the α subunit isoform is developmentally regulated and tissue specific. Sodium channels in the adult central nervous system and heart contain β1 through β4 subunits, whereas sodium channels in adult skeletal muscle have only the β1 subunit.6,7 Nav1.3 is highly expressed in embryonic sensory neurons and CNS, but its level dramatically decreases in adult rodents.8 Up-regulation of Nav1.3 channel expression was described in injured neurons and injured spinal cord.9-11
References 1. Wu, L. et al. (2002) NeuroReport 13, 2547. 2. Fang, X. et al. (2002) J. Neurosci. 22, 7425. 3. Fjell, J. et al. (2000) NeuroReport 11, 199. 4. Baker, M.D. and Wood, J.N. (2001) Trends Pharmacol. Sci. 22, 27. 5. Lai, J. et al. (2003) Curr.Opin. Neurobiol 13, 291. 6. Isom, L.L. (2001) Neuroscientist 7, 42. 7. Catterall, W.A. et al. (2003) Pharmacol Rev 55, 575. 8. Lai, J. et al. (2004) Annu. Rev. Pharmacol. Toxicol. 44, 371. 9. Hains, B.C. et al. (2003) J. Neurosci. 23, 8881. 10. Cummins, T. R. et al. (2001) J. Neurosci. 21, 5952. 11. Shah, B. S. et al. (2001) J. Physiol. 534.3, 763.
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