Anti-Peroxiredoxin SO2/3 antibody
Recognises mammalian overoxidised 2-Cys peroxiredoxin 1-4 (Prx1-4) with a strong signal and low background noise
Western blot analysis of mouse fibroblasts incubated with vehicle or 1mM H2O2 for 15 minutes
|Antibody||Anti-Peroxiredoxin SO2/3 antibody|
|Antigen Peptide||KLH conjugated synthetic peptide crb1200280e|
|Protein ID||UniProtKB - Q06830,P32119, P30048, Q13162|
|Aliases||PRDX3, Thioredoxin-dependent peroxide reductase, mitochondrial/ Antioxidant protein 1, AOP-1, HBC189, PRDX2, PRX III, Peroxiredoxin, PRP, PRX II, Natural Killer cell-enhancing factor B, NKEF-B, Thiol-specific antioxidant protein, TSA|
|Target Protein Species||Human, frog|
|Storage Stabilisers||This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/ thaw cycles.|
|Disease Area||Cancer, Circadian Rhythm|
|Specificity||PTM - oxidised form|
|Post-translational Modification||Overoxidized form of Peroxiredoxin 1-4|
|Storage||This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/ thaw cycles.|
Milev, N., Rey, G., Valekunja, U., Edgar, R., O’Neill, J. and Reddy, A. (2015). Analysis of the Redox Oscillations in the Circadian Clockwork. Methods Enzymol, 185-210. PMID: 25707278
Ishida, Y., Takikawa, M., Suzuki, T., Nagahama, M. and Ogasawara, Y. (2014). Irreversible hyperoxidation of peroxiredoxin 2 is caused by tert-butyl hydroperoxide in human red blood cells. FEBS Open Bio, 4(1), 848-852. PMID: 25379381
Park, S-J., Kim, T-S., Kim, J-M., Chang, K-T., Lee, H-S. and Lee, D-S. (2015). Repeated Superovulation via PMSG/hCG Administration Induces 2-Cys Peroxiredoxins Expression and Overoxidation in the Reproductive Tracts of Female Mice. Mol Cells, 38(12), 1071-1078. PMID: 26486164
Peroxiredoxins (Prxs) are a recently identified highly abundant and reactive family of antioxidant enzymes that reduce H2O2 via cysteine residue reactivity and make up the major cellular sink for cellular peroxides. Prxs are essential for preventing neurodegenerative disorders, haemolytic anaemia and inflammation from oxidative stress through the elimination of H2O2.
The cysteine residues of Prx1-4 proteins are converted to thioredoxin (Trx) via a sulfenic intermediate and a disulphide bridge. However due to the slow rate of conversion to the disulfide, the sulfenic intermediate is occasionally over-oxidized to cysteine sulfinic acid (Cys-SO2H) or cysteine sulfonic acid (Cys-SO3H), which leads to the inactivation of the peroxidase activity. Prx proteins exhibit circadian cycles in their oxidation status in the absence of transcription and the inactivated form of the enzyme displays circadian accumulation.
Overoxidized Prxs are also seen in excessive oxidative stress conditions such as the balloon-injured rat carotids, human atherosclerotic lesions, Pyrazole-induced liver Injury, and aged rat liver.