Scn1a Rabbit Polyclonal Antibody
Specifications
| Product Data | |
| Application | IF, IHC, WB |
|---|---|
| Recommended Dilution | WB: 1:200-1:2000; IHC: 1:100-1:3000 |
| Reactivity | Human, Mouse, Rat |
| Antibody Host | Rabbit |
| Clonality | Polyclonal |
| Immunogen | Peptide (C)TASEHSREPSAAGRLSD, corresponding to amino acid residues 465-481 of rat Nav1.1. Â ?Intracellular loop between domains I and II. |
| Buffer | Lyophilized. Concentration before lyophilization ~0.8mg/ml (lot dependent, please refer to CoA along with shipment for actual concentration). Buffer before lyophilization: phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.05% NaN3. |
| Reconstitution Method | Add 50 ul double distilled water (DDW) to the lyophilized powder. |
| Purification | Affinity purified on immobilized antigen. |
| Conjugation | Unconjugated |
| Storage | Store at -20°C as received. |
| Stability | Stable for 12 months from date of receipt. |
| Shipping | Ambient |
| Gene Name | sodium voltage-gated channel alpha subunit 1 |
| Database Link | |
| Background | Voltage-gated sodium channels (Nav) are essential for the generation of action potentials and for cell excitability. Nav channels are activated in response to depolarization and selectively allow flow of Na+ ions. To date, nine Nav a subunits have been cloned and named Nav1.1-Nav1.9. 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). 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. Na+ channels in the adult central nervous system and heart contain β1 through β4 subunits, whereas Na+ channels in adult skeletal muscle have only the β1 subunit. Nav1.1 is a highly tetrodotoxin-sensitive channel and is broadly expressed in neurons. Mutations in NaV1.1 are associated with at least two forms of epilepsy. Gain-of-function missense mutations are a primary cause of generalized epilepsy with febrile seizures plus (GEFS+). Loss-of-function mutations cause severe myoclonic epilepsy of infancy (SMEI). |
| Synonyms | FEB3; FEB3A; GEFSP2; HBSCI; NAC1; Nav1.1; SCN1; SMEI |
| Reference Data | |
Reviews
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Citations
*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen
complexities in the preparation of your product. International customers may expect an additional 1-2 weeks
in shipping.
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