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AB5580

Sigma-Aldrich

Anti-SCN8A Sodium Channel Antibody

Chemicon®, from rabbit

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Synonym(s):
Sodium Channel Nav1.6, NaCh6, PN4, CerIII
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

affinity purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

rat, mouse

manufacturer/tradename

Chemicon®

technique(s)

immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... SCN8A(6334)

General description

Voltage-gated sodium channels perform critical roles for electrical signaling in the nervous ssystem by generating action potentials in axons and dndrites. At least 10 genes encode sodium channels in mammals, but specific physiological roles that distinguish each of these isoforms are not well known. Nav1.6 is highly concentrated at notes of Ranvier of both sensory and motor axons in the peripheral nervous system and at nodes in the central nervous system. Because of its consistant and restrictied labeling, Anti-Nav1.6 (AB5580) has been used effectively as a nodes of Ranvier marker.

Specificity

Recognizes Scn8a (Nav1.6). The epitope corresponds to the intracellular loop between II and III domains of Scn8a. Does not cross react with any other known proteins.

SPECIES REACTIVITIES: It is expected that the antibody will also work on mouse (20/20) and human (19/20) due to sequence homology. Other species have not been tested.

Immunogen

Peptide corresponding to amino acids 1042-1061 from mouse (Accession number AAD20438) or rat (Accession number AAC26014) Scn8a.

Application

Detect SCN8A Sodium Channel using this Anti-SCN8A Sodium Channel Antibody validated for use in IC, IH & WB.
Western blot: (1:200) using ECL on rat brain membranes.

Immunohistochemistry on fixed frozen sections.

Immunocytochemistry on rat dorsal root ganglion primary culture (1:100)

Dilutions should be made using a carrier protein such as BSA (1-3%)

Optimal working dilutions must be determined by the end user.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Hazard Statements

Precautionary Statements

Hazard Classifications

Aquatic Chronic 3

WGK

WGK 3


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Jacy L Wagnon et al.
Neurology. Genetics, 3(4), e170-e170 (2017-07-14)
To determine the functional effect of SCN8A missense mutations in 2 children with intellectual disability and developmental delay but no seizures. Genomic DNA was analyzed by next-generation sequencing. SCN8A variants were introduced into the Nav1.6 complementary DNA by site-directed mutagenesis.
Ping Li et al.
eNeuro, 4(3) (2017-07-01)
The GABA-B receptor is densely expressed throughout the brain and has been implicated in many CNS functions and disorders, including addiction, epilepsy, spasticity, schizophrenia, anxiety, cognitive deficits, and depression, as well as various aspects of nervous system development. How one
Devid Damiani et al.
The Journal of comparative neurology, 520(7), 1406-1423 (2011-11-22)
Retinitis pigmentosa (RP) is a family of inherited diseases causing progressive photoreceptor death. Retinal ganglion cells (RGCs) form the biological substrate for various therapeutic approaches designed to restore vision in RP individuals. Assessment of survival and preservation of RGCs in
Yasmina Manso et al.
Glia, 66(1), 34-46 (2017-07-20)
Chronic cerebral hypoperfusion is a key mechanism associated with white matter disruption in cerebral vascular disease and dementia. In a mouse model relevant to studying cerebral vascular disease, we have previously shown that cerebral hypoperfusion disrupts axon-glial integrity and the
Christopher D Makinson et al.
Neuron, 93(5), 1165-1179 (2017-02-28)
Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of

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