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1 o, ZMIZ1 showed impaired coactivation of the androgen receptor.
2 required to make testosterone, nor a nuclear androgen receptor.
3 imately promote DNA double-strand breaks and androgen receptor activation in prostate epithelial cell
5 cribe the Collaborative Modeling Project for Androgen Receptor Activity (CoMPARA) efforts, which foll
7 activity that is concomitantly modulated by androgen receptor and by CCAAT/enhancer-binding protein
8 matin for steroid hormone receptors, such as androgen receptor and estrogen receptor(1-4), but mechan
10 e medium led to decreased expression of both androgen receptor and its target gene products, prostate
13 Notably, these brain regions are rich in androgen receptors and play a key role in modulating agg
16 FOXA1 in mediating oncogenesis driven by the androgen receptor, and provides mechanistic insights int
17 ty is repressed by the liganded estrogen and androgen receptors, and by the hypothalamic gonadotropin
18 ive tumours express luminal markers, such as androgen receptors, and have a lower proliferative activ
20 were divided in five groups (n = 10/group): androgen receptor antagonist (flutamide); estrogen recep
21 mide (MDV3100) is a potent second-generation androgen receptor antagonist approved for the treatment
23 fically, we bilaterally implanted the potent androgen receptor antagonist flutamide in two key brain
30 cit immune response, and the presence of the androgen receptor AR-V4 and -V7 isoforms in all NCI-60 t
33 ation of mechanisms underlying the increased androgen receptor (AR) activity and subsequent developme
35 ought to reconcile the clear contribution of androgen receptor (AR) activity that has been establishe
36 drogens control transcription by stimulating androgen receptor (AR) activity, yet also control pre-mR
39 ens in muscle, and that intervention with an androgen receptor (AR) agonist will reverse musculoskele
42 riple-negative breast cancers (TNBC) express androgen receptor (AR) and are potentially responsive to
46 ells, most prostate cancer cells express the androgen receptor (AR) and depend on androgens for their
47 link ligand chemical structures to MIEs for androgen receptor (AR) and glucocorticoid receptor (GR)
48 ed LNCaP proliferation, along with decreased androgen receptor (AR) and increased Nkx3.1 cellular exp
49 tochondrial deacetylase sirtuin 3 (SIRT3) by androgen receptor (AR) and its coregulator steroid recep
50 prostate-specific enhancers enriched for the androgen receptor (AR) and lineage-specific cofactors.
51 r develops very slowly in most men, with the androgen receptor (AR) and MYC transcription factors amo
53 at the bulk of prostate cancer cells express androgen receptor (AR) and that androgens are required f
56 s developed resistance to the new-generation androgen receptor (AR) antagonist enzalutamide is a leth
59 -C in androgen-dependent PC cells suppresses androgen receptor (AR) axis signaling and induces the ne
60 he lncRNA-p21 transcription via altering the androgen receptor (AR) binding to different androgen-res
61 nomously activates Nkx3.1 expression through androgen receptor (AR) binding to the 11-kb region in bo
63 zalutamide (Enz) can occur through bypass of androgen receptor (AR) blockade by the glucocorticoid re
64 ponsive to sex hormones, with enhancement by androgen receptor (AR) but suppression by estrogen recep
66 Alteration to the expression and activity of androgen receptor (AR) coregulators in prostate cancer i
77 e of this work was to evaluate the effect of androgen receptor (AR) inhibition on prostate-specific m
84 uman epidermal growth factor receptor 2, the androgen receptor (AR) is also a potential drug target i
85 F-1) domain located in the N-terminus of the androgen receptor (AR) is an attractive therapeutic alte
88 such as ERalpha, the activation function of androgen receptor (AR) is largely dependent on its ligan
89 ighly expressed in cancer cells in which the androgen receptor (AR) is not detected (AR-), whereas th
100 Unexpectedly, TRX1 inhibition also elevates androgen receptor (AR) levels under AD, and AR depletion
101 that the chromatin structure surrounding the androgen receptor (AR) locus is altered in the prostate
105 Since testosterone can work directly via the androgen receptor (AR) or indirectly via the estrogen re
107 ased on the expression of well-characterized androgen receptor (AR) or neuroendocrine (NE) genes: (i)
108 e-genome duplication, A. burtoni possess two androgen receptor (AR) paralogs, ARalpha and ARbeta, pro
112 onal targets of E2F, and identified that the androgen receptor (AR) played a critical role in the tra
115 d 100 cases of human melanoma and found that androgen receptor (AR) positive melanoma patients have w
120 eading cause of cancer death in men, and the androgen receptor (AR) represents the primary target for
122 (polyQ) tract polymorphism within the human androgen receptor (AR) shows population heterogeneity.
124 of the disease, is characterized by loss of androgen receptor (AR) signaling during neuroendocrine t
125 ostate cancer (PC) is initially dependent on androgen receptor (AR) signaling for survival and growth
126 ate cancer (PCa), leading to reactivation of androgen receptor (AR) signaling in a hormone-refractory
132 (mCRPC) develops resistance to inhibitors of androgen receptor (AR) signaling through a variety of me
133 cancer is characterized by a dependence upon androgen receptor (AR) signaling, and androgen deprivati
135 castration resistant prostate cancers become androgen receptor (AR) signaling-independent and develop
148 we demonstrate a direct requirement for the androgen receptor (AR) to maintain HR gene expression an
150 2 (CHK2) is a critical negative regulator of androgen receptor (AR) transcriptional activity, prostat
151 ivities of transcription factors such as the androgen receptor (AR) underpin prostate cancer developm
152 and RNA-based genomic alterations, including androgen receptor (AR) variant expression, AR transcript
153 generation of constitutively active forms of androgen receptor (AR) variants including AR-V7 plays an
154 (PCa) genomic data, and found that BMI1 and androgen receptor (AR) were positively correlated, sugge
155 denced by the dependency of PCa cells on the androgen receptor (AR), a prostate master transcription
157 scovery of highly potent PROTAC degraders of androgen receptor (AR), as exemplified by compound 34 (A
158 teins elevated in mutant ER cells, including androgen receptor (AR), chitinase-3-like protein 1 (CHI3
160 ent tumors typically remain dependent on the androgen receptor (AR), non-AR-driven tumors that also e
161 sor by targeting several proteins, including androgen receptor (AR), steroid receptor coactivator 3 (
162 xpress estrogen receptor alpha (ERalpha) and androgen receptor (AR), suggesting changing levels of go
163 As androgens mediate their actions via the androgen receptor (AR), we combined a mouse model of dih
164 s binding of beta-catenin to the promoter of androgen receptor (AR), which leads to increased express
165 drug enzalutamide by a phenotypic shift from androgen receptor (AR)-dependent luminal epithelial cell
167 TEFb (CDK9/cyclin T) plays a central role in androgen receptor (AR)-mediated transactivation by phosp
169 nce with the widespread use of highly potent androgen receptor (AR)-pathway inhibitors (APIs) such as
170 s and lymph node metastasis showing that the androgen receptor (AR)-positive ccRCC may prefer to meta
171 DOT1L selectively impaired the viability of androgen receptor (AR)-positive PCa cells and organoids,
172 tibody that internalizes in cells expressing androgen receptor (AR)-regulated prostate-specific enzym
185 the strict androgen-dependent regulation of androgen receptor (AR): binding of androgen induces stru
186 Increased expression of the full-length androgen receptor (AR-FL) and AR splice variants (AR-Vs)
187 ations with disease progression, full-length androgen receptor (AR-FL) expression, response to therap
188 ee such master regulators (FOXA1, NKX3.1 and androgen receptor, AR) in a primed conversion strategy s
189 rogenetic alopecia revealed that next to the androgen receptor as well the retinoid receptor and part
190 our results identify ALK5 and non-canonical androgen receptors as potential therapeutic targets for
191 ing cytotoxic drugs and agents targeting the androgen receptor axis, immune checkpoint receptors or D
192 ng a 6-fold difference in log-probability of androgen receptor binding at the variant rs2680708 (17q2
193 ion signature, which revealed enrichment for androgen receptor binding sequences and hypomethylation
195 ugh FOXA1, LSD1 inhibition broadly disrupted androgen-receptor binding and its transcriptional output
197 aryl pyrazol-1-yl-propanamides as selective androgen receptor degraders (SARDs) and pan-antagonists
200 n disease onset and progression through both androgen receptor-dependent and androgen receptor-indepe
203 tein expression levels of AROM, estrogen and androgen receptors did not differ between males and fema
204 ed after one to two lines of next-generation androgen receptor-directed therapy and one taxane-based
205 the steroid nuclear hormone receptor family (androgen receptor, estrogen receptor alpha, glucocortico
206 Clinically relevant Ezh2 inhibitors restore androgen receptor expression and sensitivity to antiandr
207 like subtypes were associated with increased androgen receptor expression and signaling, only luminal
209 vides a noninvasive method for assessment of androgen receptor expression in patients with metastatic
214 this group, expression of glucocorticoid and androgen receptor genes explained the most variance in t
215 androgen deprivation, downregulation of the androgen receptor -> phosphatidylinositol-3-kinase -> Ak
216 creasingly effective therapies targeting the androgen receptor have paradoxically promoted the incide
218 ernatant induce nuclear translocation of the androgen receptor in female genital skin primary culture
221 ovel mouse model with a specific ablation of androgen receptor in the adrenal cortex with or without
222 f PPARGC1a in the epithelial compartment and androgen receptor in the dermal papilla of miniaturized
223 A9) was recently characterized as a membrane androgen receptor in various teleost and mammalian cell
224 ivation by PrCa master-regulators (including androgen receptor) in Position Weight Matrix, Chip-Seq,
226 t ERG, through its physical interaction with androgen receptor, induces AR aggregation and endoplasmi
227 rase-1 plus androgen receptor is superior to androgen receptor inhibition in metastatic castration-re
230 nhanced neuritogenesis in the presence of an androgen receptor inhibitor to the extent seen in ED pep
231 Darolutamide is a structurally distinct androgen-receptor inhibitor that is approved for the tre
233 argeting poly (ADP-ribose) polymerase-1 plus androgen receptor is superior to androgen receptor inhib
234 e-cell RNAseq (scRNAseq) in the Sertoli-cell androgen receptor knockout (SCARKO) mutant and control m
236 ur transcriptome-based subtypes: (1) luminal androgen receptor (LAR), (2) immunomodulatory, (3) basal
238 asodilatation in AE-PCOS is a consequence of androgen receptor-mediated, suppressed ET(B) R-stimulate
239 describes different effects of the selective androgen receptor modulator (SARM) nandrolone phenylprop
240 only 23 (52%) contained 1 or more selective androgen receptor modulators (Ostarine, LGD-4033, or And
242 d and sold through the internet as selective androgen receptor modulators and compare the analyzed co
244 nalyses of 44 products marketed as selective androgen receptor modulators and sold via the internet,
245 g 44 products marketed and sold as selective androgen receptor modulators, only 23 (52%) contained 1
246 the increasing use of nonsteroidal selective androgen receptor modulators, which have not been approv
250 While androgens may function via nuclear androgen receptor (nAR) to increase bladder cancer (BCa)
251 t engagement, evidenced by decreased percent androgen receptor nuclear localization (%ARNL) and incre
254 NA damage/replication stress response, TP53, androgen receptor, phosphatidylinositol-3-kinase/AKT, an
255 lling of key regulatory cascades such as the androgen receptor, PI3K-AKT or GATA2-dependent pathways,
259 in prostate adenocarcinoma are driven by the androgen receptor, providing opportunities for functiona
260 arms showed comparable levels of ERG, PTEN, androgen receptor PSA, and glucocorticoid receptor expre
261 We have previously shown that miR-32 is an androgen receptor-regulated miRNA overexpressed in castr
263 n males than in females due to the different androgen receptor signaling but the molecular mechanisms
266 ts treated with a first-line next-generation androgen receptor signaling inhibitor (ARSI; abiraterone
267 ply a marker of resistance to 2nd-generation androgen receptor signaling inhibitors (ARSi) like abira
268 ated with better OS in patients treated with androgen receptor signaling inhibitors (ARSI), whereas h
269 rall survival times in patients treated with androgen receptor signaling inhibitors and taxanes.
270 and genetic experiments revealed that intact androgen receptor signaling is necessary for androgen's
271 R1 levels increase in response to suppressed androgen receptor signaling or loss of the tumor suppres
272 ncometabolite, can directly regulate nuclear androgen receptor signaling to drive tumorigenesis, ther
273 t SPOP mutation activates both PI3K/mTOR and androgen receptor signaling, effectively uncoupling the
274 nd candidate resistance mechanisms including androgen receptor signaling, mucin overexpression and an
278 on of markers associated with proliferation, androgen-receptor signaling, and hypoxia was assessed by
283 demonstrated that the constitutively active androgen receptor splice variant-7 (AR-V7) associates wi
285 We reported previously that the detection of androgen receptor splice variant-7 (AR-V7) mRNA in circu
286 Treatment-refractory, constitutively active androgen receptor splice variants promote hepatocellular
287 of cancer-specific transcripts including the androgen-receptor splice variant 7 in a cohort of prosta
291 and its transcriptional activity through the androgen receptor-STK4/MST1-protein phosphatase 2A axis,
296 e Cancer Genome Atlas revealed that YAP1 and androgen receptor transcript levels correlate with each
298 e prostate cells, including expansion of the androgen receptor transcriptional repertoire, and ERF ha
299 d response to therapy had elevated levels of androgen receptor variant 7 (ARV7) and the mesenchymal m