EC Number |
Application |
Reference |
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1.1.1.213 | diagnostics |
co-immobilization of the enzyme with diaphorase of Clostridum sp. onto alkylamine glass beads through glutaraldehyde coupling for determination of bile acids in serum and bile in a cost-effective colorimetric assay |
673967 |
1.1.1.213 | drug development |
2'-hydroxyflavanone may be useful for clinical therapy of malignancies where AKR1C3 is overexpressed like in prostate and breast cancer |
697265 |
1.1.1.213 | drug development |
the enzyme is a target for treatment of chronic pain in neuropathic diseases, overview |
689169 |
1.1.1.213 | medicine |
exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity. Pretreatment of the resistant cells with proteasome inhibitor Z-Leu-Leu-Leu-al augments the cisplatin sensitization elicited by aldo-keto reductase inhibitors |
724719 |
1.1.1.213 | medicine |
positive isoform AKR1C3 immunoreactivity is extensively present in both adenocarcinoma and squamous cell carcinoma arising from the lung and the gastroesophageal junction. Isoform AKR1C3 immunoreactivity is absent in small cell carcinoma of the lung |
725153 |
1.1.1.213 | medicine |
uniform, diffuse, and strong expression of isoform AKR1C3 in normal endometrial epithelium but not in endometrial stromal cells. The expression of AKR1C3 is reduced in both hyperplastic and carcinomatous endometrial epithelium |
725152 |
1.1.1.213 | synthesis |
the enzyme is useful in reductive production of steroids. In a coupled-enzyme system comprising HSDH and formate dehydrogenase, a twofold increase in production rate of androsterone is obtained when utilizing 1-butyl-3-methylimidazolium L-lactate with NADH regeneration |
674981 |