SOD1 ELISA Kit

Produktnummer ABIN4986813

Dieses Human SOD1 ELISA-Kit ist ein Colorimetric ELISA-Kit, das dafür entwickelt wurde, Human SOD1 zu quantifizieren.

Kurzübersicht für SOD1 ELISA Kit (ABIN4986813)

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

Reaktivität: Human

Nachweismethode: Colorimetric

Methodentyp: Sandwich ELISA

Detektionsbereich: 78-5000 pg/mL

Applikation: ELISA

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

Produktdetails SOD1 ELISA Kit

Untere Nachweisgrenze: 78 pg/mL

Analytische Methode: Quantitative

Spezifität: Natural and recombinant Human Cu/ZnSOD Ligand

Sensitivität: 40 pg/mL

Benötigtes Material:

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

Anwendungsinformationen

Applikationshinweise: Detection Wavelength: 450 nm

Probenmenge: 20 μL

Testdauer: 3 h

Plattentyp: Pre-coated

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Lagerung: 4 °C

Details zu SOD1

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

Andere Bezeichnung: Cu/ZnSOD

Hintergrund: 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