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Human Polyclonal AKR1C3 Primary Antibody for ELISA, WB - ABIN151439
Werner, Kulle, Sommerfeld, Riepe, Wudy, Hartmann, Merz, Döhnert, Bertelloni, Holterhus, Hiort: Testosterone synthesis in patients with 17β-hydroxysteroid dehydrogenase 3 deficiency. in Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation 2012
Show all 2 Pubmed References
Human Polyclonal AKR1C3 Primary Antibody for ELISA, WB - ABIN1534617
Korzekwa, Szczepańska, Bogdaszewski, Nadolski, Malż, Giżejewski: Production of prostaglandins in placentae and corpus luteum in pregnant hinds of red deer (Cervus elaphus). in Theriogenology 2016
Human Polyclonal AKR1C3 Primary Antibody for ELISA, WB - ABIN547394
Iczkowski, Qiu, Qian, Somerville, Rittmaster, Andriole, Bostwick: The dual 5-alpha-reductase inhibitor dutasteride induces atrophic changes and decreases relative cancer volume in human prostate. in Urology 2005
Human Polyclonal AKR1C3 Primary Antibody for WB - ABIN522094
Quiñones-Lombraña, Ferguson, Hageman Blair, Kalabus, Redzematovic, Blanco: Interindividual variability in the cardiac expression of anthracycline reductases in donors with and without Down syndrome. in Pharmaceutical research 2014
Human Polyclonal AKR1C3 Primary Antibody for WB - ABIN522092
Ebert, Kisiela, Wsól, Maser: Proteasome inhibitors MG-132 and bortezomib induce AKR1C1, AKR1C3, AKR1B1, and AKR1B10 in human colon cancer cell lines SW-480 and HT-29. in Chemico-biological interactions 2011
Human Polyclonal AKR1C3 Primary Antibody for FACS, WB - ABIN654117
Canzian, Cox, Setiawan, Stram, Ziegler, Dossus, Beckmann, Blanché, Barricarte, Berg, Bingham, Buring, Buys, Calle, Chanock, Clavel-Chapelon, DeLancey, Diver, Dorronsoro, Haiman, Hallmans, Hankinson, Hunter, Hüsing, Isaacs, Khaw, Kolonel, Kraft, Le Marchan: Comprehensive analysis of common genetic variation in 61 genes related to steroid hormone and insulin-like growth factor-I metabolism and breast cancer risk in the NCI breast and prostate cancer cohort consortium. in Human molecular genetics 2010
Show all 6 Pubmed References
Genotype data on the AKR1C3 rs12529 SNP indicates that all three prostate cancer groups (New Zealanders, African Americans, and Caucasian Americans) have similar genotype and allele frequencies. The highest percentage of high-risk PC as a percentage of all PC were recorded for ever-smoker AA men with the AKR1C3 rs12529 CC genotype while the lowest was recorded for never-smoker NZ men with the CG+GG genotypes.
AKR1C3 is a novel epithelial-mesenchymal transition driver in prostate cancer metastasis through activating ERK signaling.
The GG genotype of AKR1C3 rs10508293 is associated with decreased risk for preeclampsia.
AKR1C3 transcriptional regulation and its role in prostate cancer progression [review]
Overexpression of AKR1C3 could result in the accumulation of prostaglandin F2alpha (PGF2alpha), which can not only promote prostate cancer cell 's proliferation but also could enhance prostate cancer cells resistance to radiation.
The replacement of C154 with a residue possessing a bulky aromatic side-chain impairs the folding of the alpha-helix containing C154 and its neighboring secondary structures, leading to low thermostability of AKR1C3.
Data suggest that, in breast cancer cells, expression of HSD17B5 and expression of GRP78 (an apoptosis inhibitor) are strongly but negatively correlated; GRP78 knockdown decreases breast cancer cell viability whereas HSD17B5 knockdown increases cell viability and cell proliferation. (HSD17B5, 17-beta-hydroxysteroid dehydrogenase 5; GRP78, 78 kDa glucose-regulated protein)
AKR1C3 is the primary enzyme and CBR1 is a minor enzyme responsible for warfarin reduction in human liver cytosol.
the present study suggests that AKR1C1, AKR1C2, AKR1C3, and AKR1C4 are closely associated with drug resistance to both CDDP and 5FU, and that mefenamic acid, an inhibitor of AKR1C, restores sensitivity through inhibition of drug-resistance in human cancer cells.
a variant in the promoter region of HSD17B5 related to fetal androgen synthesis influences the genital phenotype in 21-Hydroxylase Deficiency females.
Five common AKR1C3 polymorphisms were associated with decreased rates of exemestane catalysis.
If our these findings can be reproduced in larger homogeneous cohorts, a genetic stratification based on the AKR1C3 rs12529 single nucleotide polymorphism, can minimize androgen deprivation therapy-related health-related quality of life effects in prostate cancer patients
We identified strong associations between the studied AKR1C3 variants and UBC risk. The homozygous variant genotype of rs12529 was found to be inversely associated with UBC, and rs1937920 was shown to be associated with increased risk of UBC. None of the genotypes were found to be significantly associated with tumor characteristics.
aldo-keto reductase 1C3-mediated prostaglandin D2 metabolism has a role in keloids
The results suggest that decreased expression of AKR1C3 may be involved in development of gastric cancer and can be restored by Sodium Butyrate.
AKR1C3 expression is elevated in prostate cancer cell lines and primary prostate cancer, suggesting a link between AKR1C3 levels and the epigenetic status in prostate cancer cells.
Aldo-keto reductase 1C3 is overexpressed in skin squamous cell carcinoma (SCC). AKR1C3 affects SCC growth via prostaglandin metabolism.
these results indicated that the actions of AKR1C3 can produce FP receptor ligands whose activation results in carcinoma cell survival in breast cancer.
and AKR1C3 may serve as a valuable therapeutic target in the treatment of castration-resistant prostate cancer
AKR1C3 activation is a critical resistance mechanism associated with enzalutamide resistance.
This gene encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reduction of prostaglandin (PG) D2, PGH2 and phenanthrenequinone (PQ), and the oxidation of 9alpha,11beta-PGF2 to PGD2. It may play an important role in the pathogenesis of allergic diseases such as asthma, and may also have a role in controlling cell growth and/or differentiation. This gene shares high sequence identity with three other gene members and is clustered with those three genes at chromosome 10p15-p14. Three transcript variants encoding different isoforms have been found for this gene.
aldo-keto reductase family 1, member C3 (3-alpha hydroxysteroid dehydrogenase, type II)
, prostaglandin F synthase
, aldo-keto reductase family 1 member C3 homolog
, 3-alpha hydroxysteroid dehydrogenase, type II
, 3-alpha-HSD type II, brain
, aldo-keto reductase family 1 member C3
, chlordecone reductase homolog HAKRb
, dihydrodiol dehydrogenase 3
, dihydrodiol dehydrogenase X
, indanol dehydrogenase
, testosterone 17-beta-dehydrogenase 5
, trans-1,2-dihydrobenzene-1,2-diol dehydrogenase
, type IIb 3-alpha hydroxysteroid dehydrogenase
, 20 alpha-hydroxysteroid dehydrogenase
, 20-alpha-hydroxysteroid dehydrogenase
, 20alpha-hydroxysteroid dehydrogenase
, aldo-keto reductase family 1 member C18
, aldo-keto reductase family 1, member C18
, 17-beta-HSD 5
, 17-beta-hydroxysteroid dehydrogenase type 5
, 3-alpha-HSD type 2
, 3-alpha-hydroxysteroid dehydrogenase type 2