Quick Order

SOD1 / Superoxide Dismutase Antibody, Mouse MAb

  • Human ADAM12 Immunoprecipitation(IP) 8029
  • Human SOD1 Flow Cytometry (FC) 5144
  • SOD1 / Superoxide Dismutase Antibody, Mouse MAb, Western blot
  • IDH1 Antibody, Mouse MAb, Flow cytometric
  • SOD1 / Superoxide Dismutase Antibody, Mouse MAb, Immunoprecipitation
  • SOD1 / Superoxide Dismutase Antibody, Mouse MAb, Flow cytometric
DatasheetReviewsRelated ProductsProtocols
Human SOD1 Antibody Product Information
Immunogen:Recombinant Human SOD1 / Superoxide Dismutase protein (Catalog#11727-H07E)
Clone ID:11
Ig Type:Mouse IgG2b
Formulation:0.2 μm filtered solution in PBS with 5% trehalose
Preparation:This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human SOD1 / Superoxide Dismutase (rh SOD1 / Superoxide Dismutase; Catalog#11727-H07E; NP_000445.1; Ala 2-Gln 154).
Human SOD1 Antibody WB Application Image
Human SOD1 Antibody FC Application Image
IDH1 Antibody, Mouse MAb, Flow cytometric
[Click to enlarge image]
Flow cytometric analysis of Human IDH1 expression in HepG2 cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and stained with Purified Mouse anti-IDH1 (12055-MM03, 1 μg/test), then a FITC-conjugated second step antibody. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Human SOD1 Antibody IP Application Image
Other SOD1 Antibody Products
SOD1 Background

SOD1 belongs to the Cu-Zn superoxide dismutase family. It binds copper and zinc ions and is one of two isozymes responsible for destroying free superoxide radicals in the body. The encoded isozyme is a soluble cytoplasmic protein, acting as a homodimer to convert naturally-occuring but harmful superoxide radicals to molecular oxygen and hydrogen peroxide. The other isozyme is a mitochondrial protein. Mutations in this gene have been implicated as causes of familial amyotrophic lateral sclerosis. Rare transcript variants have been reported for this gene. SOD1 destroys radicals which are normally produced within the cells and which are toxic to biological systems. Defects in SOD1 are the cause of amyotrophic lateral sclerosis type 1 (ALS1). ALS1 is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of cases leading to familial forms.

Human SOD1 References
  • Murakami K, et al. (2011) SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid β protein oligomerization and memory loss in mouse model of Alzheimer disease. J Biol Chem. 286(52):44557-68.
  • Thompson M, et al. (2012) Paradoxical roles of serine racemase and D-serine in the G93A mSOD1 mouse model of amyotrophic lateral sclerosis. J Neurochem. 120(4):598-610.
  • Magrané J, et al. (2012) Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons. J Neurosci. 32(1):229-42.
  • Gertz B, et al. (2012) Nuclear localization of human SOD1 and mutant SOD1-specific disruption of survival motor neuron protein complex in transgenic amyotrophic lateral sclerosis mice. J Neuropathol Exp Neurol. 71(2):162-77.
  • Product nameProduct name
    Size / Price
    Catalog: 11727-MM11-50
    List Price: 
    Price:      (You Save: )

    Datasheet & Documentation

    All information of our products is subject to change without notice. Please refer to COA enclosed in shipped package for the newest information.