SOD1 elisa pair set

SOD1 Matched ELISA Antibody Pair Set, Human

Cat. Num. AAA8118397

• Synonyms: SOD1; SOD1 Matched ELISA Antibody Pair Set; Human; Human SOD1/Superoxide Dismutase ELISA Pair Set; superoxide dismutase 1; soluble; ALS Matched ELISA Antibody Pair Set; ALS1 Matched ELISA Antibody Pair Set; HEL-S-44 Matched ELISA Antibody Pair Set; homodimer Matched ELISA Antibody Pair Set; hSod1 Matched ELISA Antibody Pair Set; IPOA Matched ELISA Antibody Pair Set; SOD Matched ELISA Antibody Pair Set; SOD1 elisa pair set

• Specificity: Quantitative determination of Human SOD1

• Assay Type: Solid Phase Sandwich ELISA
• Detection Range: 62.5-4000pg/mL
• Sensitivity: 62.5pg/ml
• Materials Provided: 1. Capture Antibody 0.2 mg/mL of mouse anti-SOD1 monoclonal antibody (in PBS, pH 7.4). Dilute to a working concentration of 2ug/mL in CBS before coating. ; 2. Detection Antibody 0.2 mg/mL rabbit anti-SOD1 polyclonal antibody conjugated to horseradish-peroxidase (HRP) (in PBS, 50 % HRP-Protector, pH 7.4). Dilute to working concentration of 0.25ug/mL in detection antibody dilution buffer before use.3. Standard Each vial contains 180 ng of recombinant SOD1. Reconstitute with 1 mL detection antibody dilution buffer. After reconstitution, store at -20 degree C to -80 degree C in a manual defrost freezer. A seven-point standard curve using 2-fold serial dilutions in sample dilution buffer, and a high standard of 4ng/mL is recommended.
• Preparation and Storage: Capture Antibody: Aliquot and store at -20 degree C to -80 degree C for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles.; Detection Antibody: Store at 4 degree C and protect it from prolonged exposure to light for up to 6 months from date of receipt. DO NOT FREEZE!; Standard: Store lyophilized standard at -20 degree C to -80 degree C for up to 6 months from date of receipt. Aliquot and store the reconstituted Standard at -80 degree C for up to 1 month. Avoid repeated freeze-thaw cycles.

Testing Data

Related Product Information for SOD1 elisa pair set

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.

This SOD1 Matched ELISA Antibody Pair Set, Human is a solid phase sandwich ELISA for quantitative determination of Human SOD1. It contains Human SOD1 capture antibody, Human SOD1 detector antibody (HRP) and a highly purified E Coli-expressed recombinant Human SOD1 protein.

References

Murakami K, et al. (2011) SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid beta 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.Magrane 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.