ライフサイエンスコーパス: transrepression

1 ds (lower GR transactivation with comparable transrepression).

2 or that adverse effects are a consequence of transrepression.

3 transactivation activity but also abolished transrepression.

4 a PPARgamma coactivator and failed to rescue transrepression.

5 tion domain competent for transactivation or transrepression.

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

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

8 enhancing the ATF3- and ICERIIgamma-mediated transrepression.

9 ethasone-induced GR transactivation, but not transrepression.

10 corepressor clearance and induction of MMP-9 transrepression.

11 receptor), a nuclear corepressor involved in transrepression.

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

13 in macrophages through a unique mechanism of transrepression.

14 nts FoxO1-PPARgamma interactions and rescues transrepression.

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

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

17 molecular mechanism termed ligand-dependent transrepression.

18 the same time on the Cyp1a1 enhancer during transrepression.

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

20 ion of this residue abolishes gamma-mediated transrepression.

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

22 ivation, suggesting SMRT does not mediate RA transrepression.

23 ession of genes either by transactivation or transrepression.

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

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

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

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

28 hereas MS6 retained both transactivation and transrepression activities.

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

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

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

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

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

34 The transrepression activity of PPAR-alpha on chronic liver

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

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

37 -binding domain completely abolished the p53 transrepression activity.

38 silencing function is not sufficient for its transrepression activity.

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

40 ally characterized as direct targets of BCL6 transrepression activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 2 AML1 C-terminal residues, which includes a transrepression domain, did not alter the activity of AM

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 ted dissociation between transactivation and transrepression in vitro.

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

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

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

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

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

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

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

98 Transrepression is widely utilized to negatively regulat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 Corticosteroids cause transrepression of certain genes, including the collagen

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

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

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

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

119 Transrepression of MMP-9 by PPARgamma and regulation by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Transrepression of TPA-induced AP-1 and transactivation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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