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Human Peroxiredoxin 2 ELISA Kit (bsk11163)  
訂購熱線:400-901-9800
訂購郵箱:sales@www.chomd.com.cn
訂購QQ:  400-901-9800
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說明書: 96T  
96T/2900.00元
大包裝/詢價
產品編號 bsk11163
英文名稱 Human Peroxiredoxin 2 ELISA Kit
中文名稱 人過氧化物酶2酶聯免疫試劑盒
別    名 MGC4104; Natural killer cell enhancing factor B; Natural killer cell-enhancing factor B; Natural Killer Enhancing Factor B; NKEF B; NKEF-B; NKEFB; Peroxiredoxin-2; PRDX 2; PRDX2; PRDX2_HUMAN; PRP; PRX2; PRXII; TDPX1; Thiol Specific Antioxidant 1; Thiol specific antioxidant protein; Thiol-specific antioxidant protein; Thioredoxin Dependent Peroxide Reductase 1; Thioredoxin Peroxidase 1; Thioredoxin-dependent peroxide reductase 1; Torin; TPX1; TSA.   
種    屬 Human
線性范圍 781.25 - 50000 pg/mL
應用范圍 S/P/CC
檢測限 390 pg/mL
適用樣品基質 cell culture supernates, serum, and plasma.
保存條件 Store at 4°C for 6 months, at -20°C for 12 months. Avoid multiple freeze-thaw cycles (Shipped with wet ice.).
注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
產品介紹 Peroxiredoxin (Prx) is an antioxidant enzyme detoxifying reactive oxygen species and has a cysteine at the active site. Prx enzymes modulate various receptor signaling pathways and protect cells from oxidatively induced death. Peroxiredoxin 1 to 4 have two conserved Cys residues corresponding to Cys51 and Cys172 of mammalian Peroxiredoxin 1. The active site cysteine(Cys51) is oxidized to cysteine sulfenic acid(Cys51-SOH) when a peroxide is reduced. Because Cys51-SOH is unstable, it forms a disulfide with Cys172-SH which comes from the other subunit of the homodimer. The disulfide is then reduced back to the Prx active thiol form by the thioredoxin-thioredoxin reductase system. However, the formation of the disulfide is a slow process. Thus under oxidative stress conditions, the sulfenic intermediate(Cys51-SOH) can be easily over oxidized to cysteine sulfinic acid(Cys-SO2H) or cysteine sulfonic acid(Cys-SO3H) before it is able to form a disulfide. Recent studies suggest that over oxidized Prx can be reduced back to the active form during recovery after oxidative stress.

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