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Key Documents

Altri documenti

S2071

Sigma-Aldrich

Anti-Sodium Channel NaV1.8 antibody produced in rabbit

affinity isolated antibody, lyophilized powder

Sinonimo/i:

Anti-PN3, Anti-SCN10A

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About This Item

Numero MDL:
MFCD08705520
Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

rabbit

Livello qualitativo

200

Coniugato

unconjugated

Forma dell’anticorpo

affinity isolated antibody

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Forma fisica

lyophilized powder

Reattività contro le specie

rat

tecniche

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

N° accesso UniProt

Q62968

Condizioni di spedizione

wet ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

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

Descrizione generale

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.

Immunogeno

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.

Applicazioni

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

Azioni biochim/fisiol

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).

Descrizione del bersaglio

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

Stato fisico

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

Esclusione di responsabilità

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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Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

nwg

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Certificati d'analisi (COA)

Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘Batch’.

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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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