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AB222957

Recombinant Human SCN3B protein (His tag)

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Recombinant Human SCN3B protein (His tag) is a Human Fragment protein, in the 23 to 159 aa range, expressed in Baculovirus infected insect cells, with >95%, < 1 EU/µg endotoxin level, suitable for SDS-PAGE.

View Alternative Names

KIAA1158, SCN3B, Sodium channel regulatory subunit beta-3

1 Images
SDS-PAGE - Recombinant Human SCN3B protein (His tag) (AB222957)
  • SDS-PAGE

Supplier Data

SDS-PAGE - Recombinant Human SCN3B protein (His tag) (AB222957)

15% SDS-PAGE analysis of 3 μg ab222957.

MWt 18-28 kDa (SDS-PAGE under reducing conditions) .

Key facts

Purity

>95% SDS-PAGE

Endotoxin level

< 1 EU/µg

Expression system

Baculovirus infected insect cells

Tags

His tag C-Terminus

Applications

SDS-PAGE

applications

Biologically active

No

Accession

Q9NY72

Animal free

No

Carrier free

No

Species

Human

Storage buffer

pH: 7.4 Constituents: PBS, 10% Glycerol (glycerin, glycerine)

storage-buffer

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }

Sequence info

[{"sequence":"ADPFPVCVEVPSETEAVQGNPMKLRCISCMKREEVEATTVVEWFYRPEGGKDFLIYEYRNGHQEVESPFQGRLQWNGSKDLQDVSITVLNVTLNDSGLYTCNVSREFEFEAHRPFVKTTRLIPLRVTEEAGEDFTSVVSEHHHHHH","proteinLength":"Fragment","predictedMolecularWeight":"16.8 kDa","actualMolecularWeight":null,"aminoAcidEnd":159,"aminoAcidStart":23,"nature":"Recombinant","expressionSystem":"Baculovirus infected insect cells","accessionNumber":"Q9NY72","tags":[{"tag":"His","terminus":"C-Terminus"}]}]

Properties and storage information

Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle
False

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

SCN3B also known as sodium channel beta-3 subunit or NaVβ3 is a protein component with a mass of approximately 21 kDa. It participates actively in the regulation of sodium ion channels which are essential for the transmission of electrical signals in the nervous system and heart. SCN3B is important for maintaining the proper functioning of various sodium channels by modulating their gating properties. It is mostly expressed in the central nervous system with significant presence noted in heart tissues. Its expression pattern suggests a role in areas requiring precise signal modulation.
Biological function summary

SCN3B influences the electrical excitability of neuronal and cardiac cells by serving as an auxiliary subunit of the voltage-gated sodium channels complex. It plays a supportive role by affecting the trafficking and functional integration of the alpha subunits which are key components for channel functionality. Through its involvement with these complexes SCN3B contributes to maintaining the balance and modulation of sodium ion flow across cell membranes which is critical for proper excitability in both neurons and myocytes.

Pathways

SCN3B's function integrates into pathways regulating electrical signaling in nerve and muscle tissues. Notably it participates in the cardiac action potential pathway ensuring that the rapid depolarization necessary for cardiac muscle contraction occurs effectively. It is also involved in the neuronal action potential signaling working closely with other proteins such as SCN1A and SCN5A which are alpha subunits of the sodium channels. These pathways highlight SCN3B's role in facilitating accurate and timely propagation of action potentials.

SCN3B abnormalities associate with conditions like Brugada syndrome and certain epileptic disorders. In Brugada syndrome a cardiac condition leading to sudden cardiac arrest SCN3B mutations can affect the sodium channels impairing signal conduction and increasing risk for arrhythmias. It has connections to SCN5A another sodium channel subunit implicated in similar cardiac disorders. For epilepsy disruptions in SCN3B can alter the excitability of neurons resulting in seizure development. By its association with key proteins SCN3B holds significant implications for understanding the molecular basis of these conditions.

Specifications

Form

Liquid

Additional notes

Affinity purified

General info

Function

Regulatory subunit of multiple voltage-gated sodium (Nav) channels directly mediating the depolarization of excitable membranes. Navs, also called VGSCs (voltage-gated sodium channels) or VDSCs (voltage-dependent sodium channels), operate by switching between closed and open conformations depending on the voltage difference across the membrane. In the open conformation they allow Na(+) ions to selectively pass through the pore, along their electrochemical gradient. The influx of Na+ ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues. The accessory beta subunits participate in localization and functional modulation of the Nav channels (PubMed : 20558140, PubMed : 21051419). Modulates the activity of SCN2A/Nav1.2, causing a hyperpolarizing shift in the voltage-dependence of inactivation of the channel and increasing the fraction of channels operating in the fast gating mode (By similarity). Modulates the activity of SCN5A/Nav1.5 (PubMed : 20558140, PubMed : 21051419, PubMed : 24567321, PubMed : 31950564). Could also regulate the atypical sodium channel SCN7A/Nav2.1 (PubMed : 35301303). Modulates the activity of SCN10A/Nav1.8, regulating its oligomerization and accelerating the recovery from inactivation (PubMed : 14975698).

Sequence similarities

Belongs to the sodium channel auxiliary subunit SCN3B (TC 8.A.17) family.

Post-translational modifications

Intramolecular disulfide bonds favor the voltage-gated sodium channel oligomeric complex assembly.. N-glycosylated.

Product protocols

Target data

Regulatory subunit of multiple voltage-gated sodium (Nav) channels directly mediating the depolarization of excitable membranes. Navs, also called VGSCs (voltage-gated sodium channels) or VDSCs (voltage-dependent sodium channels), operate by switching between closed and open conformations depending on the voltage difference across the membrane. In the open conformation they allow Na(+) ions to selectively pass through the pore, along their electrochemical gradient. The influx of Na+ ions provokes membrane depolarization, initiating the propagation of electrical signals throughout cells and tissues. The accessory beta subunits participate in localization and functional modulation of the Nav channels (PubMed : 20558140, PubMed : 21051419). Modulates the activity of SCN2A/Nav1.2, causing a hyperpolarizing shift in the voltage-dependence of inactivation of the channel and increasing the fraction of channels operating in the fast gating mode (By similarity). Modulates the activity of SCN5A/Nav1.5 (PubMed : 20558140, PubMed : 21051419, PubMed : 24567321, PubMed : 31950564). Could also regulate the atypical sodium channel SCN7A/Nav2.1 (PubMed : 35301303). Modulates the activity of SCN10A/Nav1.8, regulating its oligomerization and accelerating the recovery from inactivation (PubMed : 14975698).
See full target information SCN3B

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