Na Channel β1 Subunit Antibody [F4D21]

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IP1:100

Application
WB, IP

Reactivity
Human, Mouse, Rat

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
38 kDa

Datasheet & SDS

Biological Description

Specificity
Na Channel β1 Subunit Antibody [F4D21] detects endogenous levels of total Na Channel β1 Subunit protein.

Clone
F4D21

Synonym(s)
Sodium channel regulatory subunit beta-1, SCN1B

Background
Na⁺ channel β1 (SCN1B) is a non‑pore‑forming subunit of voltage‑gated sodium channels that combines an extracellular immunoglobulin‑like domain, a single transmembrane segment, and a short intracellular tail, and acts both as a modulator of Nav α‑subunit function and as a cell‑adhesion molecule in excitable tissues. Association of β1 with multiple Nav α‑subunits, including Nav1.1, Nav1.2, Nav1.5, and others, alters channel gating and surface density by shifting activation and inactivation properties, regulating recovery from inactivation, and promoting trafficking of α‑subunits to the plasma membrane, which changes action potential threshold, firing frequency, and conduction in neurons and cardiomyocytes. The extracellular Ig‑like domain supports homophilic and heterophilic cell–cell and cell–matrix adhesion, participates in neurite outgrowth and pathfinding, and localizes Nav complexes to specialized membrane microdomains such as axon initial segments, nodes of Ranvier, and intercalated discs, where coordinated electrical signaling is required. β1 is a substrate for regulated intramembrane proteolysis: sequential cleavage by BACE1 and γ‑secretase generates an intracellular domain that translocates to the nucleus, and transcriptomic analyses identify sets of genes whose expression depends on β1‑ICD levels, linking this fragment to transcriptional control of excitability‑related genes including those encoding Nav1.5. Loss‑of‑function variants in SCN1B reduce β1‑mediated modulation of Nav channels and remove β1‑ICD‑dependent transcriptional restraint, and are associated with developmental and epileptic encephalopathy, generalized epilepsy with febrile seizures plus, and a spectrum of focal and generalized epilepsies that carry high risk of sudden death. SCN1B pathogenic variants are also linked to Brugada syndrome, familial atrial fibrillation, and broader cardiac conduction defects, and mouse models with Scn1b deletion show severe seizures, ventricular arrhythmias, sinoatrial node dysfunction, and atrial remodeling, indicating that β1 contributes to coordinated regulation of neuronal and cardiac excitability.

Background

Na⁺ channel β1 (SCN1B) is a non‑pore‑forming subunit of voltage‑gated sodium channels that combines an extracellular immunoglobulin‑like domain, a single transmembrane segment, and a short intracellular tail, and acts both as a modulator of Nav α‑subunit function and as a cell‑adhesion molecule in excitable tissues. Association of β1 with multiple Nav α‑subunits, including Nav1.1, Nav1.2, Nav1.5, and others, alters channel gating and surface density by shifting activation and inactivation properties, regulating recovery from inactivation, and promoting trafficking of α‑subunits to the plasma membrane, which changes action potential threshold, firing frequency, and conduction in neurons and cardiomyocytes. The extracellular Ig‑like domain supports homophilic and heterophilic cell–cell and cell–matrix adhesion, participates in neurite outgrowth and pathfinding, and localizes Nav complexes to specialized membrane microdomains such as axon initial segments, nodes of Ranvier, and intercalated discs, where coordinated electrical signaling is required. β1 is a substrate for regulated intramembrane proteolysis: sequential cleavage by BACE1 and γ‑secretase generates an intracellular domain that translocates to the nucleus, and transcriptomic analyses identify sets of genes whose expression depends on β1‑ICD levels, linking this fragment to transcriptional control of excitability‑related genes including those encoding Nav1.5. Loss‑of‑function variants in SCN1B reduce β1‑mediated modulation of Nav channels and remove β1‑ICD‑dependent transcriptional restraint, and are associated with developmental and epileptic encephalopathy, generalized epilepsy with febrile seizures plus, and a spectrum of focal and generalized epilepsies that carry high risk of sudden death. SCN1B pathogenic variants are also linked to Brugada syndrome, familial atrial fibrillation, and broader cardiac conduction defects, and mouse models with Scn1b deletion show severe seizures, ventricular arrhythmias, sinoatrial node dysfunction, and atrial remodeling, indicating that β1 contributes to coordinated regulation of neuronal and cardiac excitability.

References
https://pubmed.ncbi.nlm.nih.gov/32503841/ https://pubmed.ncbi.nlm.nih.gov/33411695/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%