Scn1a Rabbit Polyclonal Antibody

Specifications

Product Data
Applications	IF, IHC, WB
Recommend Dilution	WB: 1:200-1:2000; IHC: 1:100-1:3000
Reactivity	Human, Mouse, Rat
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.
Formulation	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 Condition	Store at -20°C as received.
Gene Name	sodium voltage-gated channel alpha subunit 1
Database Link	NP_110502 Entrez Gene 6323 HumanEntrez Gene 20265 MouseEntrez Gene 81574 Rat UniProt ID P04774
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

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