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1 GRbeta also may play a role in glucocorticoid hyperrespo
2 GRbeta and FKBP51 may be responsible for increased respo
3 GRbeta does not bind glucocorticoids and is an inhibitor
4 GRbeta expression was increased at night only in NA, pri
5 GRbeta was expressed in all PV EBs but only in EBs from
8 rmed to detect the expression of GRalpha and GRbeta in TM cells and its regulation by dexamethasone (
10 cocorticoid receptor (GR) exist, GRalpha and GRbeta, which arise from alternative splicing of the GR
13 d SRp20; increased SRp30c, SRp40 levels, and GRbeta/alpha ratio, and suppressed DEX response in TM ce
14 (GRalpha) and glucocorticoid receptor beta (GRbeta), and transcripts containing different forms of e
18 n of mouse neutrophils, which do not contain GRbeta, resulted in a significant reduction in the rate
20 modulate the GR splicing process to enhance GRbeta levels and thereby decrease the GC response in cu
28 evels and determine their effects on GRalpha/GRbeta ratios as well as dexamethasone (DEX) responsiven
32 he glucocorticoid responsiveness, changes in GRbeta nuclear transport could influence subsequent resp
34 e in GRalpha mRNA and a 2.0-fold increase in GRbeta mRNA in HeLaS3 cells, which endogenously express
39 ption, and a nuclear localized beta isoform (GRbeta), which does not bind known ligands and attenuate
40 Glaucomatous TM cell strains have a lower GRbeta-GRalpha ratio compared to normal TM cells, making
42 clarify the effect of the dominant negative GRbeta isoform (unable to bind STAT-5) on erythropoiesis
46 ompletely blocks the nuclear accumulation of GRbeta and consequently leads to the degradation of GRbe
47 oduces an overexpression and accumulation of GRbeta in the nucleus with a corresponding increase in n
51 rmed to detect the subcellular expression of GRbeta and Hsp90 in normal and glaucomatous trabecular m
52 sed to compare the subcellular expression of GRbeta between normal and glaucomatous TM cell lines.
53 onclude that high constitutive expression of GRbeta by human neutrophils may provide a mechanism by w
55 ha isoform remained unchanged, expression of GRbeta, the dominant-negative GR isoform, was synergisti
56 sms proposed include increased expression of GRbeta, which competes with and thus inhibits activated
61 s of DEX and FK506 and the overexpression of GRbeta and FKBP51 on glucocorticoid-mediated gene expres
64 omatous TM cell lines, and the regulation of GRbeta in the Dex-induced reporter gene luciferase or en
65 y a mechanism involving the up-regulation of GRbeta isoform, thus providing a novel in vitro cellular
66 a mRNA is responsive to insulin, the role of GRbeta in insulin signaling and growth pathways is unkno
67 and stimulated DEX-induced translocation of GRbeta in normal TM cells, but not in glaucoma TM cells.
68 roles of FKBP51 in the nuclear transport of GRbeta and glucocorticoid responsiveness were investigat
74 d delivery of hepatic GRbeta overexpression (GRbeta-Ad) resulted in suppression of gluconeogenic gene
76 variant of the human glucocorticoid receptor GRbeta has been implicated in glucocorticoid responsiven
77 variant of the human glucocorticoid receptor GRbeta has dominant negative activity and has been impli
80 The A3669G polymorphism, which stabilizes GRbeta mRNA, had greater frequency in PV (55%; n = 22; P
81 ession of either GRbeta or FKBP51 stimulated GRbeta translocation and reduced DEX-induced luciferase
88 oimmunoprecipitation experiments verify that GRbeta complexes with Hsp90 and the microtubule motor pr
93 ely increased the steady-state levels of the GRbeta protein isoform over GRalpha, making GRbeta the p
95 rpose of this study was to determine whether GRbeta inhibits the actions of GCs in the liver, or enha
96 506 increased the association of FKBP51 with GRbeta and stimulated DEX-induced translocation of GRbet
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