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1 dently activated by aldo-keto-reductase 1C3 (AKR1C3).
2 receptors belong to the AKR1C family (AKR1C1-AKR1C3).
3 ges a noncatalytic tyrosine residue (Y24) on AKR1C3.
4 ns, and thus has the potential to counteract AKR1C3.
5 ounted by indomethacin a potent inhibitor of AKR1C3.
6 (H)2 + IL-22 such as downregulated ACER1 and AKR1C3.
7 ted androgen, 11-ketotestosterone (11KT), by AKR1C3.
8                                   This makes AKR1C3 a target for the treatment of CRPC.
9 (1500-fold) inhibitor of aldo-keto reductase AKR1C3: a target of interest in both breast and prostate
10                   These results suggest that AKR1C3 activation is a critical resistance mechanism ass
11 s demonstrated that LX compounds bind to the AKR1C3 active sites and inhibit AKR1C3 enzymatic activit
12 -vivo and in-vitro evidence of modulation of AKR1C3 activity by insulin in PCOS and in women with INS
13 ve adipose androgen generation by increasing AKR1C3 activity in female subcutaneous adipose tissue.
14    Here we assessed the effect of insulin on AKR1C3 activity in vivo and in vitro.
15                                              AKR1C3 and AKR1C1 were localized on the same myoepitheli
16 phase II inducers but not the highly related AKR1C3 and AKR1C4 family members (84% sequence homology)
17 tional inhibitors that competitively inhibit AKR1C3 and block its coactivator function could be devel
18 sed to inhibit cyclooxygenase, also inhibits AKR1C3 and displays selectivity over AKR1C1/AKR1C2.
19 ght the pro-tumoral growth of both wild-type AKR1C3 and mutant in vitro and in vivo.
20 cant time-dependent changes in expression of AKR1C3 and SRD5A1 and secretion of T/DHT.
21 etrahydrobiopterin (BH4) synthesis (CBR1 and AKR1C3) and recycling (PCBD2).
22              Homogeneous recombinant AKR1C1, AKR1C3, and AKR1C4 gave similar catalytic profiles to th
23 mes involved in androgen synthesis (CYP17A1, AKR1C3, and HSD17B6), as well as expression of full-leng
24                         Sigma/Millipore Anti-AKR1C3 antibody (mouse monoclonal, clone NP6.G6.A6) show
25                         Sigma/Millipore Anti-AKR1C3 antibody and mouse monoclonal, clone NP6.G6.A6 ca
26 al Abcam [EPR16726] and Sigma/Millipore anti-AKR1C3 antibody, mouse monoclonal, clone NP6.G6.A6, puri
27 D5A1, aldo-keto reductase family 1 member C3/AKR1C3), b) establishment of endometrial decidualization
28                                Inhibition of AKR1C3 by indomethacin, a nonsteroidal anti-inflammatory
29 lation of cellular stress markers AKR1C2 and AKR1C3 can be quantitatively measured in the presence of
30                        We further found that AKR1C3 can bind Siah2 and inhibit its self-ubiquitinatio
31                     Aldo-keto reductase 1C3 (AKR1C3) catalyzes the synthesis of 9alpha,11beta-prostag
32       All other tested biomarkers, including AKR1C3, CD3E, CD40, CD8A, CD9, CTLA4, ENTPD1, FOXP3, GZM
33 roduction of T and induction of PSA in LNCaP-AKR1C3 cells as a model of a CRPC cell line.
34  and blocked testosterone formation in LNCaP-AKR1C3 cells.
35 mediated production of testosterone in LNCaP-AKR1C3 cells.
36                                    Moreover, AKR1C3 confers chemotherapeutic resistance to the anthra
37               In contrast, overexpression of AKR1C3 confers resistance to enzalutamide.
38           Genetically manipulated cells with AKR1C3 construction were examined to highlight the pro-t
39 roid dehydrogenase, aldo-keto reductase 1C3 (AKR1C3) converts Delta(4)-androstene-3,17-dione and 5alp
40 rison with those of AKR1C1 and AKR1C2, PGFS (AKR1C3) could catalyze the reduction and/or oxidation re
41  progesterone-related genes (AKR1C1, AKR1C2, AKR1C3, CYP3A4, SRD5A1, SRD5A2, and PGR) influenced brea
42 1C1 and, to a lesser extent, AKR1C2 (but not AKR1C3) decreased progesterone-dependent PR activation o
43        To investigate the functional role of AKR1C3 during PHK differentiation, its expression and ac
44  AKR1C3 expression by shRNA or inhibition of AKR1C3 enzymatic activity by indomethacin resensitized e
45  bind to the AKR1C3 active sites and inhibit AKR1C3 enzymatic activity.
46  in CWR22Rv1 prostate cancer cells decreased AKR1C3 expression as well as intracellular androgen leve
47                                 Knockdown of AKR1C3 expression by shRNA or inhibition of AKR1C3 enzym
48                                              AKR1C3 expression correlated positively with body-mass i
49 rapy for relapsed/refractory T-ALL, and that AKR1C3 expression could be used as a biomarker to select
50  PHKs, we used immunofluorescence to examine AKR1C3 expression in AD and psoriasis lesions.
51              Insulin significantly increased AKR1C3 expression in differentiated subcutaneous adipocy
52                                          The AKR1C3 expression in peripheral blood by Protein Wes and
53  AD-associated mediator, PGD(2), upregulated AKR1C3 expression in PHKs, we used immunofluorescence to
54                                              AKR1C3 expression levels in these samples were evaluated
55                   In conclusion, blockage of AKR1C3 expression provides potential therapeutic benefit
56 analysis and quantitative PCR confirmed that AKR1C3 expression was also upregulated in differentiatio
57                                              AKR1C3 expression was measured by real-time PCR.
58  vitro, and that sensitivity correlated with AKR1C3 expression.
59 hibition of AR activity by itself stimulated AKR1C3 expression.
60      To investigate aldo-keto reductase 1C3 (AKR1C3) expression in T and B acute lymphoblastic leukem
61                     Aldo-keto reductase 1C3 (AKR1C3) has been shown to mediate the metabolism of sex
62 ree commercial antibodies were evaluated for AKR1C3 immunohistochemistry (IHC) staining performance:
63                            Overexpression of AKR1C3 in a resistant BCP-ALL xenograft resulted in dram
64         Our work demonstrates a function for AKR1C3 in differentiation-associated gene regulation and
65          However, the biological function of AKR1C3 in HCC remains unclear.
66 We observed parallel expression of Siah2 and AKR1C3 in human prostate cancer tissues.
67             Here we investigated the role of AKR1C3 in liver carcinogenesis using in vitro and in viv
68 he inducible aldo-keto reductases AKR1C2 and AKR1C3 in living human cells.
69 ght to investigate the expression pattern of AKR1C3 in normal human epidermis.
70 tively, our findings identify a new role for AKR1C3 in regulating Siah2 stability and thus enhancing
71 fluorescence revealed a strong expression of AKR1C3 in the differentiated suprabasal layers compared
72 wn cells, suggesting a nonenzymatic role for AKR1C3 in these outcomes.
73 ostenedione through aldoketoredutase type 3 (AKR1C3) in women with insulin resistance.
74 isclosure of a covalent inhibitor for potent AKR1C3 inactivation with proteome-wide selectivity in ce
75                                    Selective AKR1C3 inhibition might offer a novel therapeutic target
76 s on the phenylamino B-ring were optimal for AKR1C3 inhibition.
77 itors and the identification of 5r, a potent AKR1C3 inhibitor (IC(50) = 51 nM) with >1216-fold select
78 replaced by an ethyl group) acts as a potent AKR1C3 inhibitor that displays selectivity for AKR1C3 ov
79 ment of a sulfonyl-triazole (SuTEx) covalent AKR1C3 inhibitor that selectively engages a noncatalytic
80                               Selectivity of AKR1C3 inhibitors across the AKR family is critical sinc
81 port the continued optimization of selective AKR1C3 inhibitors and the identification of 5r, a potent
82                                    Selective AKR1C3 inhibitors are required because compounds should
83                    Two of the best selective AKR1C3 inhibitors had K(i) values of 0.1 and 2.7 muM, ex
84                                              AKR1C3 inhibitors should not inhibit AKR1C1/AKR1C2, whic
85       We report herein the identification of AKR1C3 inhibitors that demonstrate exquisite isoform sel
86 s in particular, are potent but nonselective AKR1C3 inhibitors.
87 yclooxygenase inhibitory activity but retain AKR1C3 inhibitory potency and selectivity.
88 analogues were synthesized and evaluated for AKR1C3 inhibitory potency and selectivity.
89    The aim of this study was to test whether AKR1C3 is a predictive biomarker of in vivo PR-104 sensi
90                           In adipose tissue, AKR1C3 is co-expressed with 11beta-hydroxysteroid dehydr
91                           We determined that AKR1C3 is frequently increased in HCC tissues with poor
92                                 In addition, AKR1C3 is highly expressed in metastatic and recurrent p
93                                     In CRPC, AKR1C3 is implicated in drug resistance, and enzalutamid
94                                              AKR1C3 is upregulated in CRPC where it catalyzes the for
95                     Aldo-keto reductase 1C3 (AKR1C3) is a key enzyme in the activation of both classi
96      Aldo-keto reductase family 1 member C3 (AKR1C3) is a member of the AKR superfamily of enzymes th
97                     Aldo-keto reductase 1C3 (AKR1C3) is overexpressed in castration-resistant prostat
98 cells elevated Siah2 protein levels, whereas AKR1C3 knockdown had the opposite effect.
99 ibitory activity on COX isozymes and blocked AKR1C3 mediated production of T and induction of PSA in
100 d not inhibit COX-1 or COX-2 but blocked the AKR1C3 mediated production of testosterone in LNCaP-AKR1
101 llular potency, as measured by inhibition of AKR1C3 metabolism of a known dinitrobenzamide substrate,
102                                              AKR1C3 mRNA expression was significantly higher in subcu
103                                          The AKR1C3.NADP(+).2'-des-methyl-indomethacin crystal struct
104 ceptor variants and the steroidogenic enzyme AKR1C3, offering a promising approach to combat drug res
105 covered with low muM K(i) values for AKR1C1, AKR1C3, or both.
106 50) = 51 nM) with >1216-fold selectivity for AKR1C3 over closely related isoforms.
107 R1C3 inhibitor that displays selectivity for AKR1C3 over other AKR1C enzymes.
108 emonstrate exquisite isoform selectivity for AKR1C3 over the other closely related isoforms to the or
109 ; genetically modified cell line HCT116 with AKR1C3 overexpression; Nalm and TF1 cell lines.
110 as non-catalytic dependent and the NRF2/MAFG-AKR1C3-PARP1 axis might be one of the important prolifer
111 wild-type or catalytically inactive forms of AKR1C3 partially rescued AR activity and growth defects
112 pounds targeting both the AR/AR variants and AKR1C3 pathways.
113 dimer NRF2/MAFG was able to bind directly to AKR1C3 promoter to activate its transcription.
114                                Unexpectedly, AKR1C3 re-expression in Siah2 knockdown cells elevated S
115 for cases), and the aldo-keto reductase 1C3 (AKR1C3) rs12529 genetic polymorphisms were analysed usin
116 p relative to the amine conferred pronounced AKR1C3 selectivity without loss of potency, while electr
117      Aldo-keto reductase family 1 member C3 (AKR1C3) serves as a contributor to numerous kinds of tum
118 vely the formation of 3beta-hydroxytibolone, AKR1C3 showed weak 3beta/3alpha-HSD activity, and AKR1C4
119 ereas 17beta-hydroxysteroid dehydrogenase 5 (AKR1C3) showed predominance in SC adipose tissue.
120   We observed promising treatment effects of AKR1C3 shRNA by intratumoral injection in mice.
121 genes mediating androgen metabolism (HSD3B2, AKR1C3, SRD5A1, AKR1C2, AKR1C1, and UGT2B15).
122                                     Further, AKR1C3 stabilized PARP1 by decreasing its ubiquitination
123  in aldo-keto reductase family 1, member C3 (AKR1C3), the prostatic enzyme that reduces adrenal andro
124                               For rs12387 in AKR1C3, the presence of 1 or 2 G alleles was associated
125 ic enzymes, such as aldo-keto reductase 1C3 (AKR1C3), to overcome drug resistance and improve outcome
126 criptase-PCR showed that AKR1C1, AKR1C2, and AKR1C3 transcripts were all expressed.
127 ratumoral androgen biosynthesis catalyzed by AKR1C3 (type 5 17B-hydroxysteroid dehydrogenase), which
128                     Aldo-keto reductase 1C3 (AKR1C3; type 5 17beta-hydroxysteroid dehydrogenase) is o
129                                              AKR1C3 was found to be upregulated in AD but not in psor
130 , we discovered that the tumorigenic role of AKR1C3 was non-catalytic dependent and the NRF2/MAFG-AKR
131                                Expression of AKR1C3 was significantly higher in T-ALL xenografts comp
132    One of the crucial steroidogenic enzymes, AKR1C3, was significantly elevated in enzalutamide-resis
133 somerase mRNA expression, but express AKR1C1-AKR1C3) were able to convert DHT into 3alpha- and 3beta-
134  transfected with AKR1C1 and AKR1C2, but not AKR1C3, were able to significantly inhibit a dose-depend
135 genic enzymes, including SRD5A1, SRD5A3, and AKR1C3, whereas expression of SRD5A2, CYP3A4, CYP3A5, an
136 , ligand access to PPARgamma is regulated by AKR1C3, which diverts PGD(2) metabolism away from J-seri
137  genes we found to be regulated by Siah2 was AKR1C3, which encodes a key androgen biosynthetic enzyme
138                                 In contrast, AKR1C3, which shares 84% sequence identity, and 5alpha-r
139 sistance; targeting intracrine androgens and AKR1C3 will overcome enzalutamide resistance and improve
140                 The lead compounds inhibited AKR1C3 with nanomolar potency, displayed >100-fold selec
141 ounds for the inactivation or degradation of AKR1C3 with varying degrees of selectivity among the 14
142 tify percent of nuclear immunoreactivity for AKR1C3 with varying disease involvement.
143 ased on 7 landscape genes (POLD2, CYCS, MYC, AKR1C3, YME1L1, ANXA7, and PDCD4) is associated with the

 
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