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AB5204

Sigma-Aldrich

Anti-Sodium Channel Antibody, Voltage Gated, Brain Type I

Chemicon®, from rabbit

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Synonym(s):
Nav1.1, SCN1A
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

100

antibody form

affinity purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

mouse, rat

manufacturer/tradename

Chemicon®

technique(s)

immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

NM_006920.4

UniProt accession no.

P35498

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... SCN1A(6323)

Specificity

Recognizes type I alpha subunit of VGSC. Does not cross react with any other sodium channel antigens tested so far.

SPECIES REACTIVITIES: It is expected that the antibody may also react with human due to sequence homology. Other species have not been tested.

Immunogen

Purified peptide from 465-481 of alpha subunit of rat type I voltage-gated sodium channel (VGSC) (Accession P04774).

Application

All procedures that are going to receive a full-length protein should be performed at 4C, and the following protease inhibitor mixture should be used: pepstatin A (1 μg/mL), leupeptin (1 μg/mL), aprotinin (1 μg/mL), Pefabloc SC (0.2 mM), benzamidine (0.1 mg/mL), and calpain inhibitors I and II (8 μg/mL each).

Western blot: 1:200 using ECL on rat brain membranes.

Immunohistochemistry on rat brain fixed frozen sections and mouse heart tissue.

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

Optimal working dilutions must be determined by the end user.
This Anti-Sodium Channel Antibody, Voltage Gated, Brain Type I is validated for use in IH, WB for the detection of Sodium Channel.

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

H412

Precautionary Statements

P273 - P501

Hazard Classifications

Aquatic Chronic 3

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

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Yishan Sun et al.
eLife, 5 (2016-07-28)
Dravet Syndrome is an intractable form of childhood epilepsy associated with deleterious mutations in SCN1A, the gene encoding neuronal sodium channel Nav1.1. Earlier studies using human induced pluripotent stem cells (iPSCs) have produced mixed results regarding the importance of Nav1.1
Cécile Brocard et al.
Nature medicine, 22(4), 404-411 (2016-03-15)
Upregulation of the persistent sodium current (I(NaP)) in motoneurons contributes to the development of spasticity after spinal cord injury (SCI). We investigated the mechanisms that regulate I(NaP) and observed elevated expression of voltage-gated sodium (Nav) 1.6 channels in spinal lumbar
Tun Li et al.
PLoS biology, 12(9), e1001944-e1001944 (2014-09-10)
Action potential (AP) generation in inhibitory interneurons is critical for cortical excitation-inhibition balance and information processing. However, it remains unclear what determines AP initiation in different interneurons. We focused on two predominant interneuron types in neocortex: parvalbumin (PV)- and somatostatin
Alex C Bender et al.
PloS one, 11(3), e0151538-e0151538 (2016-03-16)
Brain oscillations play a critical role in information processing and may, therefore, be essential to uncovering the mechanisms of cognitive impairment in neurological disease. In Dravet syndrome (DS), a mutation in SCN1A, coding for the voltage-gated sodium channel Nav1.1, is
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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