Nav1.5 Antibody [G4B10] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Lane 1: Mouse heart

Usage Information

Dilution
WB1:1000 IP1:50

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
230-280 kDa

Datasheet & SDS

Biological Description

Specificity
Nav1.5 Antibody [G4B10] detects endogenous levels of total Nav1.5 protein.

Clone
G4B10

Synonym(s)
Sodium channel protein type 5 subunit alpha; Sodium channel protein cardiac muscle subunit alpha; Sodium channel protein type V subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.5; hH1; SCN5A

Background
Nav1.5 (encoded by the SCN5A gene) is a voltage‑gated sodium‑channel α‑subunit of the Nav1.x family that forms the primary tetrodotoxin‑resistant Na⁺ conductance in adult cardiomyocytes and drives the rapid upstroke of the cardiac action potential and intercellular impulse propagation. The channel protein embeds in the sarcolemma as a multisubunit complex in which the Nav1.5 α‑subunit, consisting of four homologous domains each with six transmembrane segments, acts as both voltage sensor and ion‑selective pore, while β‑subunits and associated scaffolding proteins such as ankyrin‑G, syntrophin, and plakophilin‑2 modulate channel trafficking, membrane microdomain localization, and gating kinetics. Upon cardiomyocyte depolarization, voltage‑dependent movement of the S4 segments promotes opening of the pore formed by the S5–S6 segments and the intervening P‑loops, allowing a transient inward Na⁺ current that initiates fast depolarization and triggers the downstream Ca²⁺‑induced Ca²⁺ release and excitation–contraction‑coupling cascade. Post-translational modifications, including palmitoylation, phosphorylation, and ubiquitin-dependent turnover, tightly regulate Nav1.5 density and open-state behaviour. These regulatory layers integrate inputs from signalling pathways, such as PKC and CaMKII, that couple Na⁺ influx to Ca²⁺ and kinase-dependent remodelling of excitability and contractility. Mutations in SCN5A that either enhance or reduce Nav1.5‑mediated inward current underlie multiple inherited arrhythmia syndromes, including Brugada syndrome, long QT syndrome type 3, and progressive familial heart block type 1A, and acquired Nav1.5 remodeling contributes to arrhythmic substrates in heart failure and ischemic cardiomyopathy.

Background

Nav1.5 (encoded by the SCN5A gene) is a voltage‑gated sodium‑channel α‑subunit of the Nav1.x family that forms the primary tetrodotoxin‑resistant Na⁺ conductance in adult cardiomyocytes and drives the rapid upstroke of the cardiac action potential and intercellular impulse propagation. The channel protein embeds in the sarcolemma as a multisubunit complex in which the Nav1.5 α‑subunit, consisting of four homologous domains each with six transmembrane segments, acts as both voltage sensor and ion‑selective pore, while β‑subunits and associated scaffolding proteins such as ankyrin‑G, syntrophin, and plakophilin‑2 modulate channel trafficking, membrane microdomain localization, and gating kinetics. Upon cardiomyocyte depolarization, voltage‑dependent movement of the S4 segments promotes opening of the pore formed by the S5–S6 segments and the intervening P‑loops, allowing a transient inward Na⁺ current that initiates fast depolarization and triggers the downstream Ca²⁺‑induced Ca²⁺ release and excitation–contraction‑coupling cascade. Post-translational modifications, including palmitoylation, phosphorylation, and ubiquitin-dependent turnover, tightly regulate Nav1.5 density and open-state behaviour. These regulatory layers integrate inputs from signalling pathways, such as PKC and CaMKII, that couple Na⁺ influx to Ca²⁺ and kinase-dependent remodelling of excitability and contractility. Mutations in SCN5A that either enhance or reduce Nav1.5‑mediated inward current underlie multiple inherited arrhythmia syndromes, including Brugada syndrome, long QT syndrome type 3, and progressive familial heart block type 1A, and acquired Nav1.5 remodeling contributes to arrhythmic substrates in heart failure and ischemic cardiomyopathy.

References
https://pubmed.ncbi.nlm.nih.gov/29798782/ https://pubmed.ncbi.nlm.nih.gov/17727828/

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%