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S8809

Sigma-Aldrich

Monoclonal Anti-Sodium Channel, Pan antibody produced in mouse

~1 mg/mL, clone K58/35, purified immunoglobulin

Synonym(s):

Sodium Channel Antibody

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

K58/35, monoclonal

species reactivity

mammals

concentration

~1 mg/mL

technique(s)

immunohistochemistry (frozen sections): suitable
indirect immunofluorescence: 1 μg/mL using sciatic and optic nerve sections; cultured hypocampal neurons
western blot: 1 μg/mL using crude brain membrane prep (rat)

isotype

IgG1

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

General description

Voltage-gated sodium channels/VGSCs (Nav) are transmembrane proteins that are initiated by the depolarization of the membrane. They are heteromultimers with large pore-forming α-subunits and smaller β-subunits.

Specificity

The sequence recognized by this clone is identical in all known vertebrate Na+ channels. In cultured hippocampal neurons, the antibody specifically stains the axon initial segment. In sciatic and optic nerves, it stains the nodes of Ranvier.

Immunogen

synthetic peptide CTEEQKKYYNAMKKLGSKK from the intracellular III-IV loop of Na+ channels

Application

Monoclonal Anti-Sodium Channel, Pan antibody produced in mouse has been used in:
  • immunohistochemistry(1:50)
  • immunostaining (1:200)
  • immunofluorescence
  • immunocytochemistry (1:100)

Biochem/physiol Actions

Voltage-gated sodium channels/VGSCs (Nav) participates in nociceptive transmission. They play a key role in regulating the exchange between the extracellular and intracellular spaces. VGSCs are crucial for the initiation and firing of action potentials. They participate in neuronal excitability. Hence mutations in the VGSC genes results in several epileptic disorders.

Physical form

Solution in 10 mM Tris, pH 7.5, containing 0.1 m NaCl, 30% glycerol, and 15 mM sodium azide.

Legal Information

Sold under exclusive license from SUNY Stony Brook.

Disclaimer

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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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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Amanda L York et al.
eNeuro, 4(4) (2017-08-12)
The neuromuscular junction (NMJ) is a chemical synapse formed between motoneurons and skeletal muscle fibers. The vertebrate NMJ uses acetylcholine (ACh) as the neurotransmitter and features numerous invaginations of the postsynaptic muscle membrane termed junctional folds. ACh receptors (AChRs) are
Analgesic and antipyretic natural products
Shilpi JA and Uddin SJ
Annual Reports in Medicinal Chemistry, 55, 435-458 (2020)
J-C Platel et al.
Proceedings of the National Academy of Sciences of the United States of America, 102(52), 19174-19179 (2005-12-17)
Before synaptogenesis, early excitability implicating voltage-dependent and transmitter-activated channels is known to be crucial for neuronal development. We previously showed that preplate (PP) neurons of the mouse neocortex express functional Na(+) channels as early as embryonic day 12. In this
Marie K Bosch et al.
Channels (Austin, Tex.), 10(4), 297-312 (2016-02-19)
Intracellular Fibroblast Growth Factor 14 (iFGF14) and the other intracellular FGFs (iFGF11-13) regulate the properties and densities of voltage-gated neuronal and cardiac Na(+) (Nav) channels. Recent studies have demonstrated that the iFGFs can also regulate native voltage-gated Ca(2+) (Cav) channels.
Alexander Drobyshevsky et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 25(25), 5988-5997 (2005-06-25)
Disruption of oligodendrocyte lineage progression is implicated in the white-matter injury that occurs in cerebral palsy. We have previously published a model in rabbits consistent with cerebral palsy. Little is known of normal white-matter development in perinatal rabbits. Using a

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