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Myeloperoxidase (MPO) is a heme-containing enzyme and the most abundant protein in polymorphonuclear leukocytes (PMNs).1 It is composed of two subunits linked by a disulfide bridge with each subunit containing a light and a heavy polypeptide chain. It can oxidize a variety of substrates and catalyzes the formation of highly reactive (pseudo)hypohalous acids and radicals including hypochlorous acid. MPO is stored in azurophilic granules of PMNs and is released from activated or necrotic PMNs, after which it can bind to and modify acidic serum proteins, as well as recruit additional PMNs. MPO also has roles in PMN apoptosis and antimicrobial defense systems, including neutrophil extracellular traps (NETs).1,2,3 MPO-deficient mice exhibit reduced survival in a polymicrobial sepsis model, increased susceptibility to experimental autoimmune encephalomyelitis (EAE), and increased atherosclerosis in mice also deficient in the LDL receptor and fed an atherogenic diet.1,4,5 Cayman's Myeloperoxidase (mouse) Polyclonal Antibody can be used for ELISA, immunohistochemistry (IHC), and Western blot (WB) applications. The antibody recognizes MPO at approximately 80 kDa from mouse samples.
WARNING This product is not for human or veterinary use.
1. Human myeloperoxidase in innate and acquired immunity. Arch. Biochem. Biophys. 500(1), 92-106 (2010).
2. Myeloperoxidase is required for neutrophil extracellular trap formation: Implications for innate immunity. Blood 117(3), 953-959 (2011).
3. Neutrophil extracellular traps contain calprotectin, a cytosolic protein complex involved in host defense against Candida albicans. PLoS Pathog. 5(10), e1000639 (2009).
4. Mice lacking myeloperoxidase are more susceptible to experimental autoimmune encephalomyelitis. J. Neuroimmunol. 112(1-2), 97-105 (2001).
5. Increased atherosclerosis in myeloperoxidase-