ライフサイエンスコーパス: GRbeta

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

6 Transfection with a GRbeta expression construct produces an overexpression a

7 cells transfected with constitutively active GRbeta.

8 rmed to detect the expression of GRalpha and GRbeta in TM cells and its regulation by dexamethasone (

9 GRalpha and GRbeta transcripts are coordinately upregulated in CEM-C

10 ticoid receptors alpha and beta (GRalpha and GRbeta) expression, increasing GRalpha/GRbeta heterodime

11 R), which has two main isoforms (GRalpha and GRbeta).

12 cocorticoid receptor (GR) exist, GRalpha and GRbeta, which arise from alternative splicing of the GR

13 , the GR exists as two isoforms, GRalpha and GRbeta.

14 he two glucocorticoid receptors, GRalpha and GRbeta.

15 bits cortisol-mediated immunosuppression and GRbeta induction to counteract GRalpha anti-inflammatory

16 d SRp20; increased SRp30c, SRp40 levels, and GRbeta/alpha ratio, and suppressed DEX response in TM ce

17 (GRalpha) and glucocorticoid receptor beta (GRbeta), and transcripts containing different forms of e

18 nuclear transport of the non-ligand-binding GRbeta is still unknown.

19 In conclusion, GRbeta antagonizes the GC-induced signaling during fasti

20 Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3b

21 n of mouse neutrophils, which do not contain GRbeta, resulted in a significant reduction in the rate

22 Overexpression of either GRbeta or FKBP51 stimulated GRbeta translocation and red

23 modulate the GR splicing process to enhance GRbeta levels and thereby decrease the GC response in cu

24 For GRbeta, the MFI was 350 +/- 60 and 1,389 +/- 143 for PBM

25 bitory qualities that have been reported for GRbeta on GRalpha.

26 s more than a 1000-fold higher than that for GRbeta mRNA.

27 Furthermore, GRbeta-Ad mice had increased hepatic lipid accumulation

28 eractions of FKBP51 and FKBP52 with GRalpha, GRbeta, Hsp90, or dynein.

29 ased by TNFalpha and IFNgamma with a GRalpha/GRbeta ratio of 1 to 3.

30 a and GRbeta) expression, increasing GRalpha/GRbeta heterodimers, which antagonize GRalpha homodimer

31 Increased levels of GRalpha/GRbeta heterodimers were found in neutrophils as compare

32 evels and determine their effects on GRalpha/GRbeta ratios as well as dexamethasone (DEX) responsiven

33 This inversion of the GRalpha/GRbeta ratio in human neutrophils compared with PBMCs wa

34 Furthermore, hepatic GRbeta increases inflammation, which leads to hepatic li

35 Adenovirus-mediated delivery of hepatic GRbeta overexpression (GRbeta-Ad) resulted in suppressio

36 he glucocorticoid responsiveness, changes in GRbeta nuclear transport could influence subsequent resp

37 The role of Hsp90 in GRbeta transport and stability were determined with the

38 e in GRalpha mRNA and a 2.0-fold increase in GRbeta mRNA in HeLaS3 cells, which endogenously express

39 The increase in GRbeta protein expression correlated with the developmen

40 Increased GRbeta mRNA expression in neutrophils at baseline, and a

41 Increased GRbeta-GRalpha ratios were associated with decreased DEX

42 spliced dominant negative regulator isoform GRbeta.

43 ption, and a nuclear localized beta isoform (GRbeta), which does not bind known ligands and attenuate

44 Glaucomatous TM cell strains have a lower GRbeta-GRalpha ratio compared to normal TM cells, making

45 GRbeta protein isoform over GRalpha, making GRbeta the predominant endogenous receptor isoform.

46 clarify the effect of the dominant negative GRbeta isoform (unable to bind STAT-5) on erythropoiesis

47 mulated the translocation of GRalpha but not GRbeta.

48 Because nuclear GRbeta is important in regulating the glucocorticoid res

49 Increased nuclear GRbeta significantly inhibited glucocorticoid responsive

50 ompletely blocks the nuclear accumulation of GRbeta and consequently leads to the degradation of GRbe

51 oduces an overexpression and accumulation of GRbeta in the nucleus with a corresponding increase in n

52 The decreased amount of GRbeta in glaucomatous TM cells could result in enhanced

53 and consequently leads to the degradation of GRbeta in proteasomes.

54 not interact with "ligand-binding domain" of GRbeta at all.

55 rmed to detect the subcellular expression of GRbeta and Hsp90 in normal and glaucomatous trabecular m

56 sed to compare the subcellular expression of GRbeta between normal and glaucomatous TM cell lines.

57 onclude that high constitutive expression of GRbeta by human neutrophils may provide a mechanism by w

58 ncreased nocturnal airway cell expression of GRbeta, an endogenous inhibitor of steroid action.

59 ha isoform remained unchanged, expression of GRbeta, the dominant-negative GR isoform, was synergisti

60 sms proposed include increased expression of GRbeta, which competes with and thus inhibits activated

61 T-5 complexes was prevented by expression of GRbeta.

62 90 correlates with the nuclear expression of GRbeta.

63 tically significant increase in intensity of GRbeta staining to 2,497 +/- 140 (P < 0.05).

64 ormal individuals expressed higher levels of GRbeta than did glaucomatous TM cells.

65 s of DEX and FK506 and the overexpression of GRbeta and FKBP51 on glucocorticoid-mediated gene expres

66 Overexpression of GRbeta in glaucomatous TM cells inhibited DEX induction

67 Overexpression of GRbeta was conducted in glaucomatous TM cell lines, and

68 omatous TM cell lines, and the regulation of GRbeta in the Dex-induced reporter gene luciferase or en

69 y a mechanism involving the up-regulation of GRbeta isoform, thus providing a novel in vitro cellular

70 a mRNA is responsive to insulin, the role of GRbeta in insulin signaling and growth pathways is unkno

71 and stimulated DEX-induced translocation of GRbeta in normal TM cells, but not in glaucoma TM cells.

72 roles of FKBP51 in the nuclear transport of GRbeta and glucocorticoid responsiveness were investigat

73 Nuclear transport of GRbeta represents a novel mechanism through which FKBP51

74 e roles of Hsp90 in the nuclear transport of GRbeta were investigated.

75 cular chaperone for the nuclear transport of GRbeta.

76 ing were used to study the effect of TSTs on GRbeta-GRalpha ratios in human TM cell strains.

77 cells, as well as in TM cells overexpressing GRbeta.

78 d delivery of hepatic GRbeta overexpression (GRbeta-Ad) resulted in suppression of gluconeogenic gene

79 In particular, GRbeta specifically targets Akt1 in growth pathways.

80 variant of the human glucocorticoid receptor GRbeta has been implicated in glucocorticoid responsiven

81 variant of the human glucocorticoid receptor GRbeta has dominant negative activity and has been impli

82 of neutralizing antibodies to IL-13 reduced GRbeta expression by BAL macrophages.

83 The alternatively spliced GRbeta isoform acts as dominant negative regulator of cl

84 The A3669G polymorphism, which stabilizes GRbeta mRNA, had greater frequency in PV (55%; n = 22; P

85 ession of either GRbeta or FKBP51 stimulated GRbeta translocation and reduced DEX-induced luciferase

86 Coimmunoprecipitation was performed to study GRbeta-Hsp90 complexes.

87 Additionally, we found that GRbeta increased phosphorylation of Akt basally, which w

88 These data indicate that GRbeta expression and the presence of A3669G likely cont

89 We show that GRbeta expression is increased in adipose and liver tiss

90 In the present study, we show that GRbeta suppresses PTEN expression, leading to enhanced i

91 While we have previously shown that GRbeta mRNA is responsive to insulin, the role of GRbeta

92 oimmunoprecipitation experiments verify that GRbeta complexes with Hsp90 and the microtubule motor pr

93 The GRbeta isoform, however, lacks helix 12 of the ligand-bi

94 Modulation of SRp levels altered the GRbeta/alpha ratio that correlated with DEX responsivene

95 ted via the GC receptor (GR) GRalpha, as the GRbeta isoform lacks a ligand-binding domain.

96 TSTs increased the GRbeta-GRalpha ratio in TM cells.

97 ely increased the steady-state levels of the GRbeta protein isoform over GRalpha, making GRbeta the p

98 Our results demonstrate that the GRbeta/Akt1 axis is a major player in insulin-stimulated

99 ha isoform, which binds the hormone, whereas GRbeta has no known ligands.

100 rpose of this study was to determine whether GRbeta inhibits the actions of GCs in the liver, or enha

101 506 increased the association of FKBP51 with GRbeta and stimulated DEX-induced translocation of GRbet

102 thasone (DEX) and FK506 and transfected with GRbeta and FKBP51 expression vectors.