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S2071

Sigma-Aldrich

Anti-Sodium Channel NaV1.8 antibody produced in rabbit

affinity isolated antibody, lyophilized powder

Synonyme(s) :

Anti-PN3, Anti-SCN10A

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About This Item

Numéro MDL:
MFCD08705520
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

200

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

lyophilized powder

Espèces réactives

rat

Technique(s)

immunohistochemistry (frozen sections): suitable using adult rat DRG
western blot: 1:200 using rat DRG lysates

Numéro d'accès UniProt

Q62968

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... SCN10A(6336)
mouse ... Scn10a(20264)
rat ... Scn10a(29571)

Catégories apparentées

Description générale

Sodium voltage-gated channel α subunit 10 (SCN10A) codes for Nav1.8 sodium channels. It is expressed in nociceptive neurons. This gene is mapped to human chromosome 3p22.2.

Immunogène

peptide (C)EDEVAAKEGNSPGPQ corresponding to residues 1943-1957 of rat Nav1.8. This sequence has 14/15 residues identical in mouse and 7/15 residues identical in human.

Application

Anti-Sodium Channel NaV1.8 antibody has been used in immunohistochemistry and immunocytochemistry.

Actions biochimiques/physiologiques

Sodium voltage-gated channel α subunit 10 (SCN10A) plays a major role in human pain. It is involved in the pathophysiology of cerebellar deficits in MS (multiple sclerosis).

Description de la cible

Anti-Sodium Channel NaV1.8 specifically recognizes NaV1.8. Voltage-gated sodium channels (VGSCs) are present in most excitable cells. They play a crucial role in regulating the cell excitability, being primarily responsible for the

Forme physique

Lyophilized from phosphate buffered saline, pH 7.4, with 1% bovine serum albumin, and 0.05 % sodium azide.

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

13 - Non Combustible Solids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

A SCN10A SNP biases human pain sensitivity.
Duan G, et al.
Molecular Pain, 12, 1744806916666083-1744806916666083 (2016)
John N Wood et al.
Journal of neurobiology, 61(1), 55-71 (2004-09-14)
Acute, inflammatory, and neuropathic pain can all be attenuated or abolished by local treatment with sodium channel blockers such as lidocaine. The peripheral input that drives pain perception thus depends on the presence of functional voltage-gated sodium channels. Remarkably, two
William A Catterall et al.
Pharmacological reviews, 55(4), 575-578 (2003-12-06)
This summary article presents an overview of the molecular relationships among the voltage-gated sodium channels and a standard nomenclature for them, which is derived from the IUPHAR Compendium of Voltage-Gated Ion Channels. The complete Compendium, including data tables for each
Channelopathy-related SCN10A gene variants predict cerebellar dysfunction in multiple sclerosis.
Roostaei T, et al.
Neurology, 86(5), 410-417 (2016)
Tomislav Kokotović et al.
Frontiers in molecular neuroscience, 14, 720973-720973 (2021-10-15)
PR domain-containing member 12 (PRDM12) is a key developmental transcription factor in sensory neuronal specification and survival. Patients with rare deleterious variants in PRDM12 are born with congenital insensitivity to pain (CIP) due to the complete absence of a subtype
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