ライフサイエンスコーパス: R1881

1 cells in the presence of exogenous androgen (R1881).

2 f CN706 was dependent on exogenous androgen (R1881).

3 ith dihydrotestosterone or synthetic agonist R1881.

4 er concentrations of the synthetic androgen, R1881.

5 potentiated the AR response to low levels of R1881.

6 aP cells was blocked by a synthetic androgen R1881.

7 in the presence of the testosterone analogue R1881.

8 of the control after a 72-h exposure to 1 nM R1881.

9 nM concentrations of the testosterone analog R1881.

10 e to trans-activate the AR in the absence of R1881.

11 edium, but was restored with the addition of R1881, a synthetic androgen.

12 ion of 319 genes is stimulated by 24 h after R1881 addition, with a similar number (300) of genes bei

13 V.ARR(2)PB-iCasp9-infected LNCaP cells after R1881 administration and is activated after AP20187 admi

14 than the growth of LNCaP cells treated with R1881 alone.

15 Phosphorylation occurred in response to R1881 and dihydrotestosterone but weakly if at all in re

16 res of the AR ligand binding domain bound to R1881 and FXXLF or LXXLL motif peptide indicate the muta

17 -induced apoptosis of LNCaP cells in both an R1881- and AP20187-dependent manner.

18 downstream from ceramide generation because R1881 blocked cell-death induction by bacterial sphingom

19 e competes poorly for the synthetic androgen R1881, but under restrictive conditions in the hsp82 mut

20 CaP but not DU145 cells is inhibited by 1 nM R1881 compared to that of the control.

21 gen receptor (AR) (e.g. dihydrotestosterone, R1881), CPA is bulkier in structure and therefore seemin

22 Androgen (R1881) -dependent stimulation of PARP-DBD expression res

23 Although concentrations of <1 nmol/L R1881 did not induce ARE reporter activity under normoxi

24 s or phosphorylation of AKT, indicating that R1881 did not interact with survival signaling of phosph

25 apoptotic effect was seen in the presence of R1881, dihydrotestosterone, and also 17beta-estradiol wi

26 tion of apoptosis at 72 h was seen only with R1881, dihydrotestosterone, cyproterone acetate, and hyd

27 show that androgens (dihydrotestosterone and R1881) down-regulate TGF-beta1-induced expression of TGF

28 of LNCaP cells with the synthetic androgen, R1881, elevates phosphorylation of serines 16, 81, 256,

29 A production by a synthetic androgen analog (R1881) enhanced fusogenicity in androgen-responsive CaP

30 ith dihydrotestosterone (DHT), testosterone, R1881, estradiol, spironolactone, progesterone, and cort

31 positive staining in cells treated with 1 nM R1881 for 72 h.

32 apparent competitor of the radioligand [(3)H]R1881 for binding to the wild type and various mutant AR

33 LNCaP prostate-cancer cell line treated with R1881 for the identification of androgen-regulated genes

34 R1881 has no effect on the GGT activity of the androgen-

35 ept for bicalutamide, mifepristone, DHT, and R1881 in a competitive binding assay as compared to wild

36 s, an effect that is rescued by the androgen R1881 in an androgen receptor (AR)-dependent manner.

37 ificantly lower levels of androgen (10 pM of R1881) in prostate cancer cells.

38 glucocorticoid (dexamethasone) and androgen (R1881) increase MAO A promoter and catalytic activities

39 en-dependent cells with an androgen agonist, R1881, increased the AR protein level, whereas it simult

40 red by the injection of the androgen agonist R1881, indicating a positive role of androgen in HBV rep

41 ctly reducing both AR protein expression and R1881-induced AR trans-activation.

42 treatment also inhibited synthetic androgen R1881-induced nuclear localization of AR, PSA expression

43 consequence of AR antagonism, EGCG repressed R1881-induced PCa cell growth.

44 ently superior inhibitor than abiraterone of R1881-induced transcriptional activity of both wild type

45 on with high doses of the synthetic androgen R1881 led to a decrease in MCM7 binding to genomic DNA,

46 Moreover, treatment of LNCaP cells with R1881 led to a decrease in the intact FKHR protein (70 k

47 were effective at preventing binding of (3)H-R1881 (methyltrienolone, a stable synthetic androgen) to

48 racellular GSH of cells pretreated with 1 nM R1881 occur at a higher rate than in control cells, sugg

49 pable of dampening or blocking the effect of R1881 on growth.

50 ed by the nonaromatizable synthetic androgen R1881 or NGF.

51 We also provide the first demonstration that R1881 permits cell death induced by low-dose TPA in the

52 Growth of LNCaP cells treated with 1 nM R1881 plus 100 mM glycylglycine, a stimulator of GGT act

53 c-Fos and PKCdelta with shRNAs suggests that R1881 promotes cell death induced by low-dose TPA throug

54 NCaP cancer cells with a synthetic androgen (R1881) revealed that SLC45A3-ELK4, and not endogenous EL

55 se the marker protein, EGFP, is expressed in R1881-stimulated ADV.ARR(2)PB-EGFP-transduced LNCaP cell

56 R1881-stimulated proliferation was equivalent in all tra

57 at androgens (5alpha-dihydrotestosterone and R1881) suppress c-Fos protein and mRNA expression induce

58 Also, the androgen agonist R1881 suppresses the activity of a CEBPB promoter report

59 Concentrations of the synthetic androgen R1881 that correspond to physiologically relevant concen

60 of the assay was much greater than with [3H]R1881, the classical androgen receptor ligand with which

61 drogen methyl-trienolone[17alpha-methyl-(3H)-R1881 to both the LNCaP AR and the wildtype AR.

62 tive RT-PCR (Q-RT-PCR) over a time-course of R1881 treatment from 0 to 72 h.

63 ly induced in response to synthetic androgen R1881 treatment.

64 mented by treatment with synthetic androgen (R1881) unless AR is deficient or is inhibited by AR-spec

65 The sensitivity of AR activation to R1881 was also increased after hypoxia treatment.

66 m all of the tumors and cell lines bound [3H]R1881 with similar high affinity (mean Kd, 0.12 nM).