AB5204
Anti-Sodium Channel Antibody, Voltage Gated, Brain Type I
Chemicon®, from rabbit
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Nav1.1, SCN1A
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biological source
rabbit
Quality Level
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.
UniProt accession no.
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.
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.
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
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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Find documentation for the products that you have recently purchased in the Document Library.
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
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
Molecular psychiatry, 29(5), 1265-1280 (2024-01-17)
Early and progressive dysfunctions of the dopaminergic system from the Ventral Tegmental Area (VTA) have been described in Alzheimer's Disease (AD). During the long pre-symptomatic phase, alterations in the function of Parvalbumin interneurons (PV-INs) are also observed, resulting in cortical
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
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
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