Cloned (Comment) | Organism |
---|---|
gene AKR1C3, expression analysis | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
cytoplasm | - |
Homo sapiens | 5737 | - |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
(5Z,13E)-(15S)-9alpha,11alpha,15-trihydroxyprosta-5,13-dienoate + NADP+ | Homo sapiens | - |
(5Z,13E)-(15S)-9alpha,15-dihydroxy-11-oxoprosta-5,13-dienoate + NADPH + H+ | - |
? | |
(5Z,13E)-(15S)-9alpha,11beta,15-trihydroxyprosta-5,13-dienoate + NADP+ | Homo sapiens | - |
(5Z,13E)-(15S)-9alpha,15-dihydroxy-11-oxoprosta-5,13-dienoate + NADPH + H+ | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | P15121 | - |
- |
Homo sapiens | P42330 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
breast cancer cell | of invasive ductal carcinoma of the breast, immunohistochemical analysis | Homo sapiens | - |
MCF-7 cell | - |
Homo sapiens | - |
MDA-MB-231 cell | high expression level | Homo sapiens | - |
MDA-MB-453 cell | - |
Homo sapiens | - |
additional information | AKR1B1 shows decreased expression in neoplastic disease, with decreased AKR1B1 immunoreactivity in carcinoma cells compared with nonneoplastic ductal cells, suggesting that AKR1B1 activity might be suppressed in tumor cells in breast cancer tissues | Homo sapiens | - |
SK-BR-3 cell | - |
Homo sapiens | - |
SUM-185PE cell | high expression level | Homo sapiens | - |
T-47D cell | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
(5Z,13E)-(15S)-9alpha,11alpha,15-trihydroxyprosta-5,13-dienoate + NADP+ | - |
Homo sapiens | (5Z,13E)-(15S)-9alpha,15-dihydroxy-11-oxoprosta-5,13-dienoate + NADPH + H+ | - |
? | |
(5Z,13E)-(15S)-9alpha,11beta,15-trihydroxyprosta-5,13-dienoate + NADP+ | - |
Homo sapiens | (5Z,13E)-(15S)-9alpha,15-dihydroxy-11-oxoprosta-5,13-dienoate + NADPH + H+ | - |
? |
Synonyms | Comment | Organism |
---|---|---|
17beta-hydroxysteroid dehydrogenase type 5 | - |
Homo sapiens |
17betaHSD5 | - |
Homo sapiens |
AKR1B1 | - |
Homo sapiens |
AKR1C3 | - |
Homo sapiens |
More | cf. 1.1.1.21 | Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
NADP+ | - |
Homo sapiens |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | AKR1B1 shows decreased expression in neoplastic disease, AKR1B1 activity might be suppressed in tumor cells in breast cancer tissues | down |
General Information | Comment | Organism |
---|---|---|
evolution | the enzyme belongs to the aldo-keto reductase family 1 | Homo sapiens |
malfunction | administration of an AKR1C3 inhibitor significantly decreases 11beta-PGF2alpha concentrations in culture media of breast cancer cells | Homo sapiens |
metabolism | AKR1C3 is an enzyme responsible for the metabolism of steroid hormones such as androgens, progesterones and estrogens in addition to the reduction of PGD2 to 11beta-PGF2alpha | Homo sapiens |
physiological function | in breast cancer, the status of the 11alpha-PGF2alpha and 11beta-PGF2alpha cognate FP receptor is associated with adverse clinical outcome only in the AKR1C3 positive cases, immunohistochemical analysis. FP receptor-mediated functions of 11beta-PGF2alpha using FP receptor expressed MCF-7 cell line shows that 11beta-PGF2alpha treatment phosphorylates ERK and CREB and induces Slug expression through FP receptor in MCF-FP, and MCF-FP cells demonstrate decreased chemosensitivity compared to parental controls. The actions of AKR1C3, but not of AKR1B1, can produce FP receptor ligands whose activation results in carcinoma cell survival in breast cancer. 11beta-PGF2alpha stimulates phosphorylation of ERK and CREB via FP receptor. AKR1C3-dependent signaling performs through 11beta-PGF2alpha and the FP receptor, overview | Homo sapiens |
physiological function | in breast cancer, the status of the 11alpha-PGF2alpha and 11beta-PGF2alpha cognate FP receptor is associated with adverse clinical outcome only in the AKR1C3 positive cases, while there are no significant correlations between FP receptor status and any of the clinicathological parameters in AKR1B1 positive cases. AKR1B1 does not induce Slug expression | Homo sapiens |