SOD1 Kit ELISA

N° du produit ABIN4986813

Ce kit ELISA Humain SOD1 est un kit ELISA Colorimetric conçu pour quantifier Humain SOD1.

Aperçu rapide pour SOD1 Kit ELISA (ABIN4986813)

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

Reactivité: Humain

Méthode de détection: Colorimetric

Type de méthode: Sandwich ELISA

Gamme de detection: 78-5000 pg/mL

Application: ELISA

Type d'échantillon: Cell Culture Supernatant, Serum, Plasma (heparin), Plasma (citrate), Plasma (EDTA)

Détail du produit SOD1 Kit ELISA

Seuil minimal de détection: 78 pg/mL

Analytical Method: Quantitative

Specificité: Natural and recombinant Human Cu/ZnSOD Ligand

Sensibilité: 40 pg/mL

Matériel non inclus:

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

Information d'application

Indications d'application: Detection Wavelength: 450 nm

Volume d'échantillon: 20 μL

Durée du test: 3 h

Plaque: Pre-coated

Restrictions: For Research Use only

Stockage

Stock: 4 °C

Détail du antigène

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

Autre désignation: Cu/ZnSOD

Sujet: 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