475911
髓过氧化物酶，来源于人多形核白细胞
A lysosomal enzyme that catalyzes oxidations by hydrogen peroxide, including MPO-chloride-mediated killing of microbes and tumor cells, inactivation of chemotactic factors, and cross-linking of proteins.
别名:
髓过氧化物酶，来源于人多形核白细胞, MPO
产品名称
髓过氧化物酶，来源于人多形核白细胞, A lysosomal enzyme that catalyzes oxidations by hydrogen peroxide, including MPO-chloride-mediated killing of microbes and tumor cells, inactivation of chemotactic factors, and cross-linking of proteins.
SMILES string
[O+H2]O[O-]
InChI
1S/H2O3/c1-3-2/h1-2H
InChI key
JSPLKZUTYZBBKA-UHFFFAOYSA-N
biological source
human
assay
≥95% (SDS-PAGE)
form
lyophilized
specific activity
150-200 units/mg protein
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
solubility
water: soluble (volume is lot-specific and can be found on the product label)
shipped in
wet ice
storage temp.
−20°C
Quality Level
Disclaimer
毒性：标准处理（A）
General description
来自多形核白细胞的天然人髓过氧化物酶。一种对过氧化氢氧化进行催化的溶酶体酶，包括MPO-氯化物介导的微生物和肿瘤细胞杀伤、趋化因子失活和蛋白质交联。MPO催化次氯酸的形成，该次氯酸通过将卤素离子与细胞内成分结合或通过细菌脂质和蛋白质的氧化来杀死细菌。
Other Notes
Nauseef, W.M., et al. 1998.J. Leukocyte Biol. 63, 264.
Panasenko, O.M., et al. 1994.Free Radic.Biol. Med. 16, 143.
Mulligan, M.S., et al. 1992.Br. J. Pharmacol.107, 1159.
Sharonov, B.P., and Churilova, I.V.1992.Biochem.Biophys.Res. Commun.189, 1129.
Panasenko, O.M., et al. 1994.Free Radic.Biol. Med. 16, 143.
Mulligan, M.S., et al. 1992.Br. J. Pharmacol.107, 1159.
Sharonov, B.P., and Churilova, I.V.1992.Biochem.Biophys.Res. Commun.189, 1129.
一个单位定义为在 25°C，pH 6.0 下，每分钟还原1.0 µmol H₂O₂的酶量。
Physical form
在100-700 mM NaCl，50 mM醋酸钠缓冲液，pH 6.0中冻干。
Preparation Note
在100 mM NaCl、50 mM醋酸钠、pH值6.0中进一步稀释。酶可能会从低离子强度缓冲液或蒸馏的H₂O中的溶液中沉淀出来。
复溶后，等分并冷冻保存（-20°C或-70°C）。贮备液在-20°C或-70°C下可稳定保存至多1年。
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
signalword
Danger
hcodes
pcodes
Hazard Classifications
Resp. Sens. 1
存储类别
11 - Combustible Solids
wgk
WGK 1
Shobini Jayaraman et al.
Biochimica et biophysica acta. Molecular and cell biology of lipids, 1865(8), 158712-158712 (2020-04-15)
Low-density lipoprotein (LDL) binding to arterial proteoglycans initiates LDL retention and modification in the arterial wall, triggering atherosclerosis. The details of this binding, its effectors, and its ramifications are incompletely understood. We combined heparin affinity chromatography with biochemical, spectroscopic and
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