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1                                              GRalpha and GRbeta transcripts are coordinately upregula
2                                              GRalpha undergoes steroid-dependent nuclear translocatio
3 veness by inhibiting steroid induced both 1) GRalpha-DNA binding activity and 2) GC-responsive elemen
4 ly increased by TNFalpha and IFNgamma with a GRalpha/GRbeta ratio of 1 to 3.
5 acological doses of L-carnitine can activate GRalpha and, through this mechanism, regulate glucocorti
6 ch competes with and thus inhibits activated GRalpha; increased secretion of macrophage migration inh
7 or the nuclear transport of ligand-activated GRalpha.
8 ), were tested for their abilities to affect GRalpha trafficking.
9  the isoforms glucocorticoid receptor alpha (GRalpha) and glucocorticoid receptor beta (GRbeta), and
10 tive levels of the active GC receptor alpha (GRalpha) and the alternatively spliced dominant negative
11 TCF, JunD and glucocorticoid receptor alpha (GRalpha), that show different enrichment patterns for pe
12               Glucocorticoid receptor-alpha (GRalpha) and peroxisome proliferator-activated receptor-
13 -carnitine on glucocorticoid receptor-alpha (GRalpha) functions.
14                             We have analyzed GRalpha and 11beta-HSD1 expression in skeletal myoblasts
15 induced nuclear factor kappaB activation and GRalpha phosphorylation, which were prevented by inhibit
16 tation experiments revealed that MUC1-CT and GRalpha form protein complexes and translocate to the nu
17 ession in vivo by both GRalpha-dependent and GRalpha-independent mechanisms.
18 in kinase phosphatase 1 gene expression, and GRalpha nuclear translocation.
19 ional co-activation of androgen receptor and GRalpha by Hic-5 in a kinase-independent manner.
20 Ralpha/GRbeta heterodimers, which antagonize GRalpha homodimer binding on IL10, DUSP1, and NFKBIA pro
21         Physiologically, hGRbeta antagonized GRalpha's function and attenuated hepatic gluconeogenesi
22 h does not bind known ligands and attenuates GRalpha action.
23 tes glucocorticoid receptors alpha and beta (GRalpha and GRbeta) expression, increasing GRalpha/GRbet
24                                         Both GRalpha transactivation and cytokine suppression by L-ca
25 nts of liver gene expression in vivo by both GRalpha-dependent and GRalpha-independent mechanisms.
26 ed in constitutive nuclear transport of both GRalpha and -beta in the absence of ligands.
27 fully reversed rhinovirus impairment of both GRalpha nuclear translocation and the transactivation/tr
28 lls were used to show binding of PP5 to both GRalpha and PPARgamma.
29              A 1757-bp 3' fragment of bovine GRalpha cDNA was also amplified from bovine lens.
30  as dominant negative regulator of classical GRalpha transcriptional activity.
31                                 The complete GRalpha sequence was obtained from rLECs and was found t
32 ppression and GRbeta induction to counteract GRalpha anti-inflammatory signaling.
33                                      MUC1-CT-GRalpha complex was downregulated in NP-CR tissue.
34 in cells from severe asthma, and the MUC1-CT/GRalpha complex was downregulated in severe asthma cells
35 he human glucocorticoid receptor (GR) exist, GRalpha and GRbeta, which arise from alternative splicin
36  (MFI) using immunofluorescence analysis for GRalpha was 475 +/- 62 and 985 +/- 107 for PBMCs and neu
37  protein isoforms: a cytoplasmic alpha form (GRalpha), which binds hormone, translocates to the nucle
38 promoter and on the expression of functional GRalpha by the cell.
39 ped localize green fluorescent protein-fused GRalpha in the cytoplasm in the absence of ligand and po
40 ling is coordinated via the GC receptor (GR) GRalpha, as the GRbeta isoform lacks a ligand-binding do
41                             Increased GRbeta-GRalpha ratios were associated with decreased DEX-mediat
42 comatous TM cell strains have a lower GRbeta-GRalpha ratio compared to normal TM cells, making them m
43 e used to study the effect of TSTs on GRbeta-GRalpha ratios in human TM cell strains.
44                    TSTs increased the GRbeta-GRalpha ratio in TM cells.
45  green fluorescent protein (GFP)-fused human GRalpha and transactivate the glucocorticoid-responsive
46  human ERK8 as a negative regulator of human GRalpha, acting through Hic-5, and suggest a broader rol
47            This was associated with impaired GRalpha nuclear translocation, as assessed by means of b
48                                 Importantly, GRalpha expression was unaffected by variations in in vi
49                                 No change in GRalpha expression was observed.
50 ry VKH patients had an impaired elevation in GRalpha expression (P = .03).
51 romoter that leads to a 1.5-fold increase in GRalpha mRNA and a 2.0-fold increase in GRbeta mRNA in H
52  (GRalpha and GRbeta) expression, increasing GRalpha/GRbeta heterodimers, which antagonize GRalpha ho
53 emokine production and its ability to induce GRalpha nuclear translocation and GRE-dependent GILZ exp
54                          Fluticasone-induced GRalpha nuclear translocation, phosphorylation at serine
55 ly, through its 14-3-3 protein interactions, GRalpha may influence these processes.
56 ntaining the N-terminal truncated GR isoform GRalpha-D3 lacking the K310 SUMOylation site, revealed a
57  receptor (GR), which has two main isoforms (GRalpha and GRbeta).
58 ive splicing, the GR exists as two isoforms, GRalpha and GRbeta.
59 in the corticosteroid response that mediates GRalpha nuclear translocation.
60 teroid resistance process, inhibiting normal GRalpha nuclear function.
61 ly modulates the lipometabolic activities of GRalpha and PPARgamma.
62 o suppressed the transcriptional activity of GRalpha on a glucocorticoid-responsive promoter.
63  trafficking and transactivation activity of GRalpha, whereas introduction of a mutation inactivating
64 ly influence the transcriptional activity of GRalpha.
65                         The concentration of GRalpha mRNA is more than a 1000-fold higher than that f
66 -3-3sigma bound the ligand-binding domain of GRalpha through its COOH-terminal portion, in a partiall
67 at raised skeletal muscle cell expression of GRalpha and 11beta -HSD1-mediated regulation of intracel
68 is was performed to detect the expression of GRalpha and GRbeta in TM cells and its regulation by dex
69  were evident between myoblast expression of GRalpha under basal conditions and levels of insulin res
70 wn and potential new biological functions of GRalpha.
71                  PP5-dependent impairment of GRalpha function represents a novel mechanism driving GC
72  bind glucocorticoids and is an inhibitor of GRalpha activity.
73                          Increased levels of GRalpha/GRbeta heterodimers were found in neutrophils as
74     Loss of PP5 increased phosphorylation of GRalpha at serines 212 and 234 and elevated dexamethason
75  shuttling and transactivation properties of GRalpha in a cell line replete with or devoid of 14-3-3s
76                                Regulation of GRalpha and 11beta-HSD1 by cortisol was abolished by the
77                Transcriptional regulation of GRalpha and interaction with its ligand binding domain b
78          DEX stimulated the translocation of GRalpha but not GRbeta.
79 6 did not alter DEX-induced translocation of GRalpha.
80 te SRp levels and determine their effects on GRalpha/GRbeta ratios as well as dexamethasone (DEX) res
81 lities that have been reported for GRbeta on GRalpha.
82 te levels of the GRbeta protein isoform over GRalpha, making GRbeta the predominant endogenous recept
83 cle (ASM) caused by a defect in GC receptor (GRalpha) function.
84 ression of the two glucocorticoid receptors, GRalpha and GRbeta.
85 increase steroid responsiveness by reversing GRalpha phosphorylation.
86 ly transfected red fluorescent protein (RFP)-GRalpha NTM5 cell lines were developed.
87                                          RFP-GRalpha receptor behaves similarly to the wild-type GRal
88                                          RFP-GRalpha translocation was temperature sensitive, occurri
89 on; however, 17AAG prevented DEX-induced RFP-GRalpha nuclear translocation.
90 ine blocked DEX-induced or RU486-induced RFP-GRalpha nuclear translocation; however, 17AAG prevented
91 nuclear import and export of DEX-induced RFP-GRalpha were faster than RU-486-induced nuclear shuttlin
92                  Nuclear localization of RFP-GRalpha in NTM5 cells treated with vehicle (ethanol), de
93                        Nuclear export of RFP-GRalpha was studied using confocal microscopy following
94 ad no effect on nuclear translocation of RFP-GRalpha.
95              NTM5 cells transfected with RFP-GRalpha showed a clear cytosolic localization of recepto
96                   These studies suggest that GRalpha transcripts containing exons 1A3, 1B, and 1C con
97                                          The GRalpha in hLECs and rLECs was shown to be transcription
98 ression by L-carnitine were abrogated by the GRalpha-antagonist RU 486.
99 ding of glucocorticoid signaling is from the GRalpha isoform, which binds the hormone, whereas GRbeta
100                        This inversion of the GRalpha/GRbeta ratio in human neutrophils compared with
101  nondenaturing conditions, we found that the GRalpha isoform coprecipitates with NF-ATc in nuclear ex
102    When equal amounts of the cDNAs for these GRalpha variant proteins are transfected into cells, the
103 e whole cell binding of [3H]dexamethasone to GRalpha by decreasing the affinity of this receptor for
104  receptor behaves similarly to the wild-type GRalpha with its cytosolic localization and shuttling to
105  the GC-induced signaling during fasting via GRalpha and the PPARalpha-FGF21 axis that reduces fat bu
106 h inhibitory actions of GCs are mediated via GRalpha, a hormone-induced transcription factor.
107  revealed that MUC4beta forms a complex with GRalpha in the nuclei of NP epithelial cells from cortic
108 form transcriptionally active complexes with GRalpha, whereas in PV EBs, STAT-5 was constitutively ph
109 study interactions of FKBP51 and FKBP52 with GRalpha, GRbeta, Hsp90, or dynein.

 
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