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人 CBR1 抗体对
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人 CBR1 抗体对

01AB03298

Carbonyl reductase 1 (CBR1) is a cytosolic NADPH-dependent oxidoreductase belonging to the short-chain dehydrogenase/reductase family. It catalyzes the reduction of a wide array of carbonyl compounds, including quinones, prostaglandins, and xenobiotics such as the anthracycline chemotherapeutics doxorubicin and daunorubicin. By converting these drugs into their cardiotoxic alcohol metabolites, CBR1 significantly influences clinical outcomes in cancer therapy. The enzyme also participates in glucocorticoid metabolism and can reduce S-nitrosoglutathione. Clinically, CBR1 is associated with Down syndrome due to its location on chromosome 21, and its activity levels are a key determinant of susceptibility to anthracycline-induced cardiotoxicity and cardiometabolic disease.

Human
规格起售价
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技术参数

靶点基因名
CBR1
基因别名
CBR; CRN; SDR21C1
蛋白别名
carbonyl reductase 1; CBR1
UniProt
P16152
物种
Human

产品详情

靶点名称
CBR1
蛋白名称
carbonyl reductase 1
蛋白别名
Carbonyl reductase [NADPH] 1; 15-hydroxyprostaglandin dehydrogenase [NADP(+]; 20-beta-hydroxysteroid dehydrogenase; Alcohol dehydrogenase [NAD(P)+] CBR1; NADPH-dependent carbonyl reductase 1; Prostaglandin 9-ketoreductase; PG-9-KR; Prostaglandin-E(2) 9-reductase; Short chain dehydrogenase/reductase family 21C member 1
靶点基因名
CBR1
基因别名
CBR; CRN; SDR21C1
UniProt
P16152
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Carbonyl reductase 1 (CBR1) is a cytosolic NADPH-dependent oxidoreductase belonging to the short-chain dehydrogenase/reductase family. It catalyzes the reduction of a wide array of carbonyl compounds, including quinones, prostaglandins, and xenobiotics such as the anthracycline chemotherapeutics doxorubicin and daunorubicin. By converting these drugs into their cardiotoxic alcohol metabolites, CBR1 significantly influences clinical outcomes in cancer therapy. The enzyme also participates in glucocorticoid metabolism and can reduce S-nitrosoglutathione. Clinically, CBR1 is associated with Down syndrome due to its location on chromosome 21, and its activity levels are a key determinant of susceptibility to anthracycline-induced cardiotoxicity and cardiometabolic disease.