SOD1 ELISA Kit

Catalog No. ABIN4986813

This Human SOD1 ELISA Kit is a Colorimetric ELISA Kit designed to quantify Human SOD1.

Quick Overview for SOD1 ELISA Kit (ABIN4986813)

Target: SOD1 (Superoxide Dismutase 1, Soluble (SOD1))

Reactivity: Human

Detection Method: Colorimetric

Method Type: Sandwich ELISA

Detection Range: 78-5000 pg/mL

Application: ELISA

Sample Type: Cell Culture Supernatant, Serum, Plasma (heparin), Plasma (citrate), Plasma (EDTA)

Product Details SOD1 ELISA Kit

Minimum Detection Limit: 78 pg/mL

Analytical Method: Quantitative

Specificity: Natural and recombinant Human Cu/ZnSOD Ligand

Sensitivity: 40 pg/mL

Material not included:

• Microplate reader.
• Pipettes and pipette tips.
• EP tube Deionized or distilled water.

Application Details

Application Notes: Detection Wavelength: 450 nm

Sample Volume: 20 μL

Assay Time: 3 h

Plate: Pre-coated

Restrictions: For Research Use only

Handling

Storage: 4 °C

Target Details for SOD1

Target: SOD1 (Superoxide Dismutase 1, Soluble (SOD1))

Alternative Name: Cu/ZnSOD

Background: Superoxide Dismutases (SODs), originally identified as Indophenoloxidase (IPO), are enzymes that catalyze the conversion of naturallyoccuring but harmful superoxide radicals into molecular oxygen and hydrogen peroxide. Superoxide Dismutases 1, SOD1, also known as Cu/Zn SOD, soluble SOD and IPOA, is a soluble, cytoplasmic 16 kDa homodimer. Each SOD1 monomer binds one Cu2+ and one Zn2+ ion. Three isozymes of SOD have been identified and are functionally related but have very modest sequence homology. SOD1 shares 23 % and 27 % sequence identity with SOD2 and SOD3, respectively. Mutations in SOD1 have been implicated as causes of familial amyotrophic lateral sclerosis (ALS). The ALScausing mutations of SOD1 are scattered throughout the protein and provide no clear functional or structural clues to the underlying disease mechanism. The oligomerization hypothesis suggests that mutant SOD1 proteins become misfolded and consequently oligomerize into high molecular weight aggregates that result in the death of motor neurons. The oxidative damage hypothesis suggests that loss of function mutation in SOD1 protein results in the accumulation of cellular superoxide radical, leading to free radicalmediated damage, the release of cytochrome c, and apoptosis.

Pathways: Sensory Perception of Sound, Transition Metal Ion Homeostasis