Any feedback?
Please rate this page
(search_result.php)
(0/150)

BRENDA support

Refine search

Search Application

show results
Don't show organism specific information (fast!)
Search organism in taxonomic tree (slow, choose "exact" as search mode, e.g. "mammalia" for rat,human,monkey,...)
(Not possible to combine with the first option)
Refine your search

Search term:

Results 1 - 5 of 5
EC Number Application Commentary Reference
Show all pathways known for 1.1.1.64Display the word mapDisplay the reaction diagram Show all sequences 1.1.1.64diagnostics evaluation of 17beta-HSD3 enzymatic activity using androgen receptor-mediated transactivation is important for understanding and diagnosing the 46,XY disorder of sexual development caused by mutations of HSD17B3 genes which results in low testosterone production. A method is adapted that easily evaluates enzymatic activity of 17beta-HSD3 by quantifying the conversion from androstenedione to trestosterone using androgen receptor-mediated transactivation 761760
Show all pathways known for 1.1.1.64Display the word mapDisplay the reaction diagram Show all sequences 1.1.1.64drug development testosterone is converted to 5alpha-dihydrotestosterone, which is present at high concentrations in patients with castration resistant prostate cancer (CRPC). Inhibition of 17beta-HSD5 is therefore considered to be a promising therapy for treating CRPC. High-throughput inhibitor screening, overview 739797
Show all pathways known for 1.1.1.64Display the word mapDisplay the reaction diagram Show all sequences 1.1.1.64medicine 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
Show all pathways known for 1.1.1.64Display the word mapDisplay the reaction diagram Show all sequences 1.1.1.64medicine 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
Show all pathways known for 1.1.1.64Display the word mapDisplay the reaction diagram Show all sequences 1.1.1.64medicine 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
Results 1 - 5 of 5