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S2071

Sigma-Aldrich

Anti-Sodium Channel NaV1.8 antibody produced in rabbit

affinity isolated antibody, lyophilized powder

Sinónimos:

Anti-PN3, Anti-SCN10A

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About This Item

Número MDL:
MFCD08705520
Código UNSPSC:
12352203
NACRES:
NA.41

origen biológico

rabbit

Nivel de calidad

200

conjugado

unconjugated

forma del anticuerpo

affinity isolated antibody

tipo de anticuerpo

primary antibodies

clon

polyclonal

formulario

lyophilized powder

reactividad de especies

rat

técnicas

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

Nº de acceso UniProt

Q62968

Condiciones de envío

wet ice

temp. de almacenamiento

−20°C

modificación del objetivo postraduccional

unmodified

Información sobre el gen

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

Descripción general

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.

Inmunógeno

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.

Aplicación

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

Acciones bioquímicas o fisiológicas

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).

Descripción de destino

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

Forma física

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

Cláusula de descargo de responsabilidad

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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Código de clase de almacenamiento

13 - Non Combustible Solids

Clase de riesgo para el agua (WGK)

nwg

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Visite la Librería de documentos

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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