ライフサイエンスコーパス: R5020

1 proget itself or the high affinity PR ligand R5020.

2 act with PRB in the presence of R5020 and MK+R5020.

3 y down-regulated by MEKK1 plus the progestin R5020.

4 cally up-regulated by EGF in the presence of R5020.

5 al and inducible sites to the same extent as R5020.

6 most promising compounds for the PR (RBA of R5020 = 100) were 16alpha,17alpha-[(R)-1'-alpha-(5-bromo

7 cyclin E, and p21(WAF1), are up-regulated by R5020 alone, they are synergistically up-regulated by EG

8 ntially interact with PRB in the presence of R5020 and MK+R5020.

9 g cells eliminated the stimulatory effect of R5020 and progesterone on GLP-1 secretion.

10 for the first 6 days post-hCG in TRL, TRL + R5020, and TRL + DHT.

11 trogens fulvestrant and tamoxifen, progestin R5020, antiprogestin RU486, all-trans-retinoic acid, epi

12 that following treatment with the progestin, R5020, breast cancer cells undergo a "biochemical shift"

13 s identified as a protein enriched in the MK+R5020 data set, and it was demonstrated that 14-3-3sigma

14 in overall phosphorylation of PR induced by R5020, demonstrating that the failure of this antagonist

15 In addition, FAK degradation was coupled to R5020-dependent turnovers of PRA and PRB.

16 The antiprogestin RU486 blocked the R5020 effect on IRS-2 expression.

17 periments, PR in the presence of the agonist R5020 exhibits rapid exchange with the MMTV promoter in

18 lly increased by epidermal growth factor and R5020 in cells expressing wild-type PR, but not S294A PR

19 e population by the synthetic progestin (Pg) R5020 in luminal breast cancer cells both in vitro and i

20 by progesterone and the synthetic progestin R5020 in MCF-7 and other progesterone receptor (PR) posi

21 Independently of EGF, R5020 increases Stat5 protein levels, association of Sta

22 n-regulation and are resistant to MEKK1-plus-R5020-induced transcriptional synergy but respond to pro

23 noted that cycloheximide partially inhibits R5020 induction of E2F1 expression, indicating that the

24 robustly induced by the progesterone agonist R5020, leading to a dramatically higher RANKL expression

25 The IRS-2 induction by R5020 occurred via an increase of IRS-2 mRNA levels.

26 progesterone (P4) or the synthetic progestin R5020 on ERK1/2 phosphorylation were independent of the

27 ethylstilbestrol, or moxestrol, but not with R5020 or dihydrotestosterone, prevented the nuclear conc

28 Significantly, PR bound to R5020 or RU486 can recruit the SWI/SNF chromatin remodel

29 synthesis inhibitor, trilostane (TRL); TRL + R5020; or TRL + dihydrotestosterone propionate (DHT).

30 factor (EGF)-stimulated signaling pathways: R5020 potentiates the effects of EGF by up-regulating EG

31 1-Dimethyl-19-norpregna-4,9-dien-3,20-dione (R5020) progestin limited this effect and was counteracte

32 r cells treated with the synthetic progestin R5020 revealed a subset of progesterone receptor (PR) ta

33 As compared to the progestin agonist R5020, RU486 stimulated a similar increase in overall in

34 othesis, we demonstrated that treatment with R5020 significantly increases both hyperphosphorylation

35 onal hyperactivity in response to MEKK1 plus R5020; stabilization of PR by inhibition of the 26S prot

36 tion of p42/p44 MAPK only in the presence of R5020, supporting a shift in the regulation of these cel

37 invasion and tube formation more than MK or R5020 treatment alone.

38 To determine the ramifications of MK+R5020 treatment on angiogenesis, in vitro assays were pe

39 o assays were performed and combinatorial MK+R5020 treatment significantly decreased endothelial cell

40 MK-2206 (MK), in conjunction with progestin (R5020) treatment, is sufficient to upregulate a subset o