Render Target: STATIC
Render Timestamp: 2024-12-09T11:33:48.146Z
Commit: 224419269841c11382c4555dbee545259bf6c379
XML generation date: 2024-08-01 15:29:30.014
Product last modified at: 2024-12-06T12:15:15.428Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

SOD1 (E4G1H) XP® Rabbit mAb #37385

Filter:
  • WB
  • IHC

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 16-18
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunohistochemistry (Paraffin) 1:200 - 1:800

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.



    For a carrier-free (BSA and azide free) version of this product see product #65778.

    Protocol

    Specificity / Sensitivity

    SOD1 (E4G1H) XP® Rabbit mAb recognizes endogenous levels of total SOD1 protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human SOD1 protein.

    Background

    SOD1, Cu/Zn superoxide dismutase, is a major antioxidant enzyme that catalyzes the conversion of superoxide anion to hydrogen peroxide and molecular oxygen (1). SOD1 is ubiquitously expressed and is localized in the cytosol, nucleus, and mitochondrial intermembrane space. The SOD1 gene locus is on chromosome 21 in a region affected in Down Syndrome (2). In addition, over 100 distinct SOD1 inherited mutations have been identified in the familial form of amyotrophic lateral sclerosis (ALS), a progressive degenerative disease of motor neurons (3-5). Despite the fact that SOD1 helps to eliminate toxic reactive species, its mutations in ALS have been described as gain-of-function (5). The mechanism by which mutant SOD1 induces the neurodegeneration observed in ALS is still unclear. Mutant SOD1 proteins become misfolded and consequently oligomerize into high molecular weight species that aggregate and end up in proteinaceous inclusions (5).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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