
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.
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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.