ライフサイエンスコーパス: transrepression

1 ds (lower GR transactivation with comparable transrepression).

2 ivation, suggesting SMRT does not mediate RA transrepression.

3 ession of genes either by transactivation or transrepression.

4 or that adverse effects are a consequence of transrepression.

5 transactivation activity but also abolished transrepression.

6 a PPARgamma coactivator and failed to rescue transrepression.

7 tion domain competent for transactivation or transrepression.

8 of SRC-1-like factors in CBP recruitment and transrepression.

9 IIB indicate likely role(s) in active and/or transrepression.

10 enhancing the ATF3- and ICERIIgamma-mediated transrepression.

11 C response element (IR nGRE)-mediated direct transrepression.

12 3C1 via activating protein-1 (AP-1)-mediated transrepression.

13 ethasone-induced GR transactivation, but not transrepression.

14 corepressor clearance and induction of MMP-9 transrepression.

15 receptor), a nuclear corepressor involved in transrepression.

16 OGT is an important component of GR-mediated transrepression.

17 in macrophages through a unique mechanism of transrepression.

18 nts FoxO1-PPARgamma interactions and rescues transrepression.

19 n domain of p53 and a reduced I(0.5) for p53 transrepression.

20 molecular mechanism termed ligand-dependent transrepression.

21 the same time on the Cyp1a1 enhancer during transrepression.

22 red for interactions with Sin3A/HDAC1 or for transrepression.

23 ion of this residue abolishes gamma-mediated transrepression.

24 ne-induced GR transactivation and NF kappa B transrepression.

25 transactivation and IR nGRE-mediated direct transrepression activities of GCs may preferentially exe

26 uclear translocation and the transactivation/transrepression activities of glucocorticoids.

27 hages and are required for nearly all of the transrepression activities of liver X receptors (LXRs),

28 he transactivation and SUMOylation-dependent transrepression activities of LXRs can be independently

29 hereas MS6 retained both transactivation and transrepression activities.

30 ns, while still exerting a tethered indirect transrepression activity and could therefore be clinical

31 is increased and that this abolishes its GR-transrepression activity and promotes corticosteroid ins

32 Despite a proposed transrepression activity of HBx(2-21), our study reveals

33 ion acceptor sites of AR does not affect the transrepression activity of PIASy on AR.

34 r PIASy-AR interaction, is essential for the transrepression activity of PIASy.

35 PIASy-Stat1 interaction, is required for the transrepression activity of PIASy.

36 The transrepression activity of PPAR-alpha on chronic liver

37 also corrects defective transactivation and transrepression activity of R496 mutant GRs.

38 agonists, selectively modulating PPAR-alpha transrepression activity, could thus be an option to pre

39 -binding domain completely abolished the p53 transrepression activity.

40 silencing function is not sufficient for its transrepression activity.

41 EKLF-PIAS3 interaction, is required for the transrepression activity.

42 ally characterized as direct targets of BCL6 transrepression activity.

43 ng agents, hypoxia-induced p53 has primarily transrepression activity.

44 Moreover, in contrast to the transrepression afforded by wild-type STAT3alpha, a STAT

45 inhibited glucocorticoid-dependent NF-kappaB transrepression and attenuated the glucocorticoid-depend

46 n macrophages at early time points, exerting transrepression and decreased TNF-alpha expression.

47 for residues 53 and 54 of p53 in regulating transrepression and demonstrates that 25-26 and 53-54 wo

48 hing a requirement for both proteins for LXR transrepression and enabling inflammatory signaling path

49 C response element (IR nGRE)-mediated direct transrepression and for tethered indirect transrepressio

50 in a significant reduction of p53-dependent transrepression and hypoxia-induced apoptosis.

51 ombination via two mechanisms: p53-dependent transrepression and p53/MDM2-mediated proteasomal degrad

52 e reporter assays of glucocorticoid-mediated transrepression and predicted response to ICS through lo

53 In contrast, NF-kappaB transrepression and RAFTK phosphorylation were not requi

54 the ability of a mutant construct to mediate transrepression and the amount of protein that it synthe

55 deacetylase 3 (HDAC3), Dex-induced tethered transrepression and the formation of a repressing comple

56 effects of steroids are thought to be due to transrepression and the side effects, transactivation.

57 or (GR) ligands that distinguish between the transrepression and transactivation activity of the GR,

58 r binding affinities, cellular activities of transrepression and transactivation, and anti-inflammato

59 nd are considered "dissociated" between gene transrepression and transactivation.

60 egrees of in vitro dissociation between gene transrepression and transactivation.

61 studies identify a molecular mechanism of GR transrepression, and highlight the function of O-GlcNAc

62 lated with a PA + PPARalpha combination, the transrepression appears to be a global phenomenon.

63 otent activity that glucocorticoids have for transrepression (as measured by inhibition of IL-1 induc

64 In contrast to transactivation, 4HPR in transrepression assays functions mostly with RARalpha, R

65 We find that although transrepression between ER and NF-kappaB does occur, pos

66 acetylase inhibitors, reverses hPRA-mediated transrepression but does not convert hPRA to a transcrip

67 RU 24858 exerts strong AP-1 inhibition (transrepression), but little or no transactivation.

68 (ID) within human PR, which is necessary for transrepression by hPRA, has been identified.

69 -dependent clearance pathway is sensitive to transrepression by liver X receptors, while the CaMKII-d

70 indings are consistent with a model in which transrepression by PPARgamma is achieved by targeting CB

71 f Merm1 impaired both GR transactivation and transrepression by reducing GR recruitment to its bindin

72 The molecular mechanism of AP-1 transrepression by retinoids is unclear, especially as r

73 ed by gene transfer suggested that NF-kappaB transrepression could contribute to apoptosis in dexamet

74 the PAH2 domain of mammalian Sin3A with the transrepression domain (SID) of human Mad1 reveals that

75 2 AML1 C-terminal residues, which includes a transrepression domain, did not alter the activity of AM

76 , containing a Kruppel-associated box (KRAB) transrepression domain, the C/EBPalpha DNA-binding domai

77 ator that possesses both transactivation and transrepression domains and/or functions.

78 id receptor (GR) agonist assay (representing transrepression effects) over an MMTV GR agonist assay (

79 results suggest that in vitro separation of transrepression from transactivation activity does not t

80 CpdX-D3 selectively activate the GR indirect transrepression function and are as effective as synthet

81 Thus the innate FoxO1 transrepression function enables insulin to augment PPAR

82 mined and each was found to exhibit a strong transrepression function in the context of the DNA bindi

83 RIF3 or its two isoforms did not relieve the transrepression function mediated by their corresponding

84 the NFkappaB/AP1-mediated tethered indirect transrepression function of the glucocorticoid receptor

85 tivation of its GC-induced indirect tethered transrepression function results in beneficial anti-infl

86 site in RepD1 (Ser(28) to Ala) abolishes its transrepression function, suggesting that the coregulato

87 e apoptotic function of p53 is linked to its transrepression function.

88 ely modulating the GR by only triggering its transrepression function.

89 e element (GRE) binding, and transactivation/transrepression functional readouts were evaluated by us

90 es establish overlapping transactivation and transrepression functions of PPARgamma and PPARdelta in

91 th the direct transactivation and the direct transrepression functions of the GC receptor (GR), where

92 is well understood, less is known about the transrepression functions of this protein.

93 m, we have uncoupled the transactivation and transrepression functions of this protein.

94 transactivation and IR nGRE-mediated direct transrepression functions, while still exerting a tether

95 rase, TAT, and glutamine synthetase, GS) and transrepression (IL-6).

96 ternal 15 amino acid domain of YY1 mediating transrepression in the viral promoter setting was identi

97 ted dissociation between transactivation and transrepression in vitro.

98 aB/AP1-mediated GC-induced tethered indirect transrepression in vitro.

99 aired p53 function (both transactivation and transrepression) in these cells.

100 EF-1 in BeWo cells alleviated TEF-1-mediated transrepression, indicating that the TBP-TEF-1 interacti

101 uces GR-driven transactivation while leaving transrepression intact.

102 We conclude that autoinhibition and transrepression involve N-terminal sumoylation combined

103 rved region of c-Myc implicated in mediating transrepression is absolutely required for c-Myc-acceler

104 e involvement of Brd4 in transactivation and transrepression is common to different types of E2 prote

105 p53 transrepression is correlated with local H3K9me3 chromat

106 The data indicate that TEF-1 transrepression is mediated by direct interactions with

107 hough the precise mechanism of hPRA-mediated transrepression is not fully understood, an inhibitory d

108 Transrepression is widely utilized to negatively regulat

109 ransactivation (FK506-binding protein 5) and transrepression markers (IL-8 and TNF-alpha) were measur

110 We demonstrate that, unlike the established transrepression mechanism in which the glucocorticoid re

111 Furthermore, we show that GR-mediated transrepression observed at TRE sites to be DNA-binding-

112 -kappaB target genes, COX-2 and IL-8 P4-PRWT transrepression occurred at the level of transcription i

113 ctions and argue against the hypothesis that transrepression occurs through competition for a single

114 noic acid receptor (RAR) transactivation and transrepression of 12-O-tetradecanoylphorbol-13-acetate-

115 new set of events takes place beginning with transrepression of a subset of inflammatory-response gen

116 This effect was independent of transrepression of activator protein-1.

117 er these data support a role for ER-mediated transrepression of AHR-dependent gene regulation.

118 eraction surface is not directly involved in transrepression of AP-1 activity.

119 vate gene expression and in part through the transrepression of AP-1 and NF-kappaB.

120 g dimers may constitute one target of RA for transrepression of AP-1.

121 bition of translation are required for Pdcd4 transrepression of AP-1.

122 Such transrepression of BSEP by E2 in vitro and in vivo requi

123 transactivation but similar steroid-induced transrepression of CD8(+) cells compared with CD4(+) cel

124 into S phase is the release of E2F-mediated transrepression of cell cycle genes, not transactivation

125 Corticosteroids cause transrepression of certain genes, including the collagen

126 genous GATAD2B significantly reduced P4-PRWT transrepression of COX-2 and IL-8 Notably, GATAD2B expre

127 pha and LXRbeta plays a critical role in the transrepression of IFN-gamma-induced STAT1-dependent inf

128 feedback loop, p53 mediates transcriptional transrepression of inducible nitric oxide synthase.

129 rved as the predominant model of GR-mediated transrepression of inflammatory genes.

130 Transrepression of MMP-9 by PPARgamma and regulation by

131 These data suggest that transrepression of NF-kappaB and AP-1 occurs through dis

132 GR mutant capable of distinguishing between transrepression of NF-kappaB and AP-1.

133 gamma is capable of regulating M-CSF through transrepression of NF-kappaB binding at the promoter.

134 h the glucocorticoid response element (GRE), transrepression of NF-kappaB, phosphorylation of RAFTK (

135 ciated with changes in dexamethasone-induced transrepression of NF-kappaB.

136 ards against DNA damage through p53-mediated transrepression of NOS2 gene expression, thus reducing t

137 ists to antagonize inflammatory responses by transrepression of nuclear factor kappa B (NF-kappaB) ta

138 ater than 10-fold selective for LXR-mediated transrepression of proinflammatory gene expression versu

139 lates WUE by modulating stomatal density via transrepression of SDD1.

140 tivation domain, is required for GR-mediated transrepression of TGF-beta transactivation.

141 ssion of COX-2 transcription in part through transrepression of the AP-1 transcription factor.

142 pression of c-Myb transactivation results in transrepression of the c-Myb promoter through the Myb re

143 PPARgamma-mediated transrepression of the MMP-9 gene was dependent on the p

144 the protein which induce transactivation or transrepression of the target genes.

145 Previous studies have suggested that transrepression of these factors by nuclear receptors in

146 issue- and gene-specific transactivation and transrepression of thousands of target genes.

147 Transrepression of TPA-induced AP-1 and transactivation

148 ropose a mechanism of AHRR action involving "transrepression" of AHR signaling through protein-protei

149 GR regardless of whether these mutants were transrepression or activation defective.

150 of apoptosis, and G(1)-S checkpoint, but not transrepression or regulation of a centrosomal checkpoin

151 ter the expression of target genes either by transrepression or transactivation.

152 Intriguingly, the LXR transrepression pathway can itself be inactivated by inf

153 gs provide evidence for an ADIOL/ERbeta/CtBP-transrepression pathway that regulates inflammatory resp

154 Overexpression of OGT potentiates the GR transrepression pathway, whereas depletion of endogenous

155 h atRA-dependent RAR transactivation or AP-1 transrepression, possibly through titration of essential

156 r receptors effect gene- and signal-specific transrepression programs remain poorly understood.

157 We found that MS4 had transrepression properties but lacked transactivation ab

158 e GR restored GRE transactivation, NF-kappaB transrepression, RAFTK phosphorylation, Bim induction, a

159 Transrepression refers to the ability of PR-A to suppres

160 e specificity and functional consequences of transrepression remain poorly understood.

161 p53-dependent transactivation and transrepression require its interaction with p300/CBP, a

162 hospho-GRIP1 and CDK9 are not detected at GR transrepression sites near pro-inflammatory genes.

163 ct transrepression and for tethered indirect transrepression that is mediated by DNA-bound NF-kappaB/

164 re are three current models for suppression: transrepression via GR tethering to AP-1/NF-kappaB sites

165 s GR-mediated transactivation but induces GR transrepression via inhibition of several transcription

166 -binding domain mutant (PRmDBD), P4-mediated transrepression was significantly reduced, suggesting a

167 B6 P+ cells, the retinoids specific for AP-1 transrepression were inhibitory, whereas SR11235, which