Superoxide dismutase enzyme prepared from bovine erythrocytes. Cells from immunisedmice were fused with cells of the mouse Sp-2/0-Ag14 myeloma cell line.
SOD1
Reactivity: Human, Mouse, Rat
WB, ELISA, ICC, IHC (p), FACS, IHC (fro), IF (p), IF (cc)
Host: Rabbit
Polyclonal
unconjugated
Application Notes
ELISA. Immunohistochemistry on Frozen Sections. Immunohistochemistry on Paraffin Sections: This product does not require pre-treatmentof paraffin embedded sections e. g. trypsin or pronase prior to staining. This product doesnot require antigen retrieval using heat treatment methods prior to staining of paraffinsections. Recommended Positive Control: Human spleen and lymph node. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user.
Restrictions
For Research Use only
Concentration
1.0 mg/mL
Buffer
PBS containing 0.09 % Sodium Azide as preservative and 0.1 % BSA as stabilizer
Preservative
Sodium azide
Precaution of Use
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C/-20 °C
Storage Comment
Store the antibody undiluted at 2-8 °C for one month or (in aliquots) at -20 °C for longer. Avoid repeated freezing and thawing. Shelf life: one year from despatch.
Superoxide dismutases are ubiquitous metalloproteins that destroy oxygen-mediated free radicals, that are normally produced within the cells, which are toxic to biological systems. There are three forms of superoxide dismutase, including the Fe, mitochondrial (Mn) and the copper/zinc binding (Cu/Zn) form. The Cu/Zn form of SOD is utilised by most eukaryotic organisms. SOD Cu/Zn prevents oxygen-mediated free radical damage by catalysing the dismutation of the toxic superoxide radical to molecular oxygen and hydrogen peroxide. Superoxide dismutatses catalyzes the conversion of single electron reduced species of molecular oxygen to hydrogen peroxide and oxygen. Cu, Zn superoxide dismutase (SOD1) is widely distributed and comprises 90 % of total SOD. Mutations in SOD1 cause a form of familial ALS. Oxidative modifications and aggregation of SOD1 has been associated with Alzheimer's and Parkinson's disease.Synonyms: ALS1, CuZn-SOD, CuZnSOD, IPOA, SOD-1, Superoxide dismutase [Cu-Zn]