ライフサイエンスコーパス: HIV-1 LTR

1 HIV-1 LTR has evolved to both highjack the T-cell activa

2 Tat-mediated transactivation of HIV type 1 (HIV-1) LTR.

3 BIV and human immunodeficiency virus type 1 (HIV-1) LTRs to levels similar to those with their homolo

4 w level of overall transcription from the 5' HIV-1-LTR.

5 In similar assays using a HIV-1 LTR construct with the core enhancer elements dele

6 NA element, in the absence of Tat, activated HIV-1 LTR expression.

7 glutinin of the transcription mediated by an HIV-1 LTR fragment containing the p53 and NF-kappaB site

8 e shown that ICP0 not only transactivates an HIV-1 LTR mutant that is unresponsive to NF-kappaB and T

9 sis, SP-A augmented both IL-6 production and HIV-1 LTR activity.

10 6 resulted in cooperative inhibition of both HIV-1 LTR-driven gene expression and HIV-1 replication.

11 yed to obtain cooperative inhibition of both HIV-1 LTR-driven gene expression and HIV-1 replication.

12 hed stable cellular transformant, containing HIV-1-LTR-reporter gene constructs, TAR-independent tran

13 ut, when expressed at high levels, decreased HIV-1 LTR expression due to cytotoxic effects.

14 Indeed, the Tat-stimulated kappaB-defective HIV-1 LTR had a markedly impaired response to GRIP1, whe

15 member produced in THP-1 macrophages during HIV-1 LTR repression.

16 FoxP3 enhances HIV-1 LTR via its specific NFkappaB binding sequences in

17 transcriptional activators are necessary for HIV-1 LTR activity in monocytes/macrophages.

18 These data indicate that p38 is required for HIV-1 LTR activation but that the action of p38 is delay

19 s-linking or exogenous IL-2 was required for HIV-1 LTR circle formation in resting CD4+ T cells.

20 1168c (PPE17) can augment transcription from HIV-1 LTR in monocyte/macrophage cells.

21 ion protein-mediated transactivation of Gal4-HIV-1 LTR with TAR deleted.

22 gnificant inhibition of HIV-1 replication in HIV-1 LTR-PKR cDNA transduced clones (105-10 : 239 and 1

23 clear factor-kappaB (NF-kappaB) resulting in HIV-1 LTR trans-activation.

24 ruitment of TBP is one rate-limiting step in HIV-1 LTR transcription and whether Tat functions to rec

25 Histone acetylation renders the inactive HIV-1 LTR responsive to NF-kappaB, indicating that a sup

26 sm by which mycobacterial protein(s) induces HIV-1 LTR trans-activation is not clearly understood.

27 e found that the host protein Naf1 inhibited HIV-1 LTR-driven transcription of HIV genes and contribu

28 to modulate the activation of an integrated HIV-1 LTR and revealed that the most potent individual a

29 at the chromatin structure of the integrated HIV-1 LTR plays a critical role in modulating basal tran

30 High level HIV-1--LTR stimulation was also achieved when IL-1beta,

31 Maximal HIV-1--LTR stimulation required both lymphocyte-derived

32 8, and LFA-1 inhibited PMN membrane-mediated HIV-1 LTR derepression.

33 PT16H or SSRP1 protein enhances Tat-mediated HIV-1 LTR (long terminal repeat) promoter activity.

34 t phorbol myristate acetate- or Tat-mediated HIV-1 LTR activation in a transient transfection system,

35 a known CTD kinase, human Cdk8, to modulate HIV-1 LTR-driven gene expression upon directed targeting

36 n which 5'-truncated or site-directed mutant HIV-1 LTR-CAT reporters were tested for their response t

37 Analyses of HIV-1 LTR deletion mutants have shown that ICP0 not only

38 Analysis of HIV-1 LTR deletion mutants demonstrated that retinoids w

39 upport of the hypothesis that enhancement of HIV-1 LTR transcription by Vpr is an indirect effect of

40 Moreover, Vpr-mediated enhancement of HIV-1 LTR-driven transcription was observed in cycling p

41 f reverse transcription and the formation of HIV-1 LTR circles (indicating nuclear import), we explor

42 ion, we found there was a 3-fold increase of HIV-1 LTR-driven luciferase expression in cord T lymphoc

43 Previous reports indicate that repression of HIV-1 LTR-directed gene expression by E1A 243R is mediat

44 TAR and prevents Tat-mediated stimulation of HIV-1 LTR transcription in vitro but has no influence on

45 d transactivator, Tat, in the stimulation of HIV-1 LTR-directed transcription.

46 ly inhibited Tat mediated transactivation of HIV-1 LTR transcription in a cell culture system.

47 ble to block Tat-mediated transactivation of HIV-1 LTR transcription in vivo as judged by the extent

48 nhibition of Tat-mediated transactivation of HIV-1 LTR.

49 a glial cell line increased transcription of HIV-1 LTR by a TAR dependent mechanism.

50 V-1 gene expression in infected cells and on HIV-1 LTR activation in transfected cells.

51 The inhibitory effect of CAF on HIV-1 LTR activation is mediated through STAT1 activatio

52 d to interact with TLR2 but had no effect on HIV-1 LTR trans-activation because of its inability to a

53 assays revealed that HspBP1 was recruited on HIV-1 LTR at NF-kappaB enhancer region (kappaB sites).

54 tions at histone H3K27 and H3R26 orchestrate HIV-1 LTR-mediated transcription, and potentially opens

55 Thus, like cellular promoters, HIV-1 LTR can use P-TEFb function without a Tat/TAR RNA

56 roducing CD4 T cells by binding the proximal HIV-1 LTR and augmenting HIV-1 transcription in partners

57 NF-kappaB/NFAT binding sites in the proximal HIV-1 LTR.

58 EBPbeta isoform and coincidentally repressed HIV-1 LTR transcription.

59 t phases of the cell cycle demonstrated that HIV-1 LTR expression was highest in G2.

60 The HIV-1 LTR-driven luciferase expression correlated with H

61 ection assays, ZF5 was shown to activate the HIV-1 LTR and repress the beta-actin promoter.

62 by CK2, blocked its ability to activate the HIV-1 LTR in response to LPS.

63 ence homology to hTat, does not activate the HIV-1 LTR, and is not active in human cells that effecti

64 om indigenous bacteria that can activate the HIV-1 LTR, cytokine production, and NF-kappaB in cells o

65 ut maintained its capability to activate the HIV-1 LTR, to localize to the nucleus and to promote non

66 uCycT1 and MuCycT1 can robustly activate the HIV-1 LTR.

67 ts suggest a role for LANA in activating the HIV-1 LTR through association with cellular molecules ta

68 Here we show that also the HIV-1 LTR promoter exploits G-quadruplex-mediated transc

69 ract with a suboptimal amount of Tat and the HIV-1 LTR for efficient initiation of viral gene transcr

70 or central to the regulation of IL-6 and the HIV-1 LTR.

71 nd Tat-mediated transactivation, such as the HIV-1 LTR with the enhancer deleted (-83 LTR) and TAR de

72 ith this finding, we identified HDAC3 at the HIV-1 LTR by chromatin immunoprecipitation.

73 the local histone acetylation levels at the HIV-1 LTR while T(3) treatment reverses this reduction.

74 In pre-initiation complexes formed at the HIV-1 LTR, the C-terminal domain (CTD) of RNA polymerase

75 on at the interleukin-2 locus but not at the HIV-1 LTR.

76 al analyses indicate that p50:RelA binds the HIV-1 LTR tandem kappaB sites with an apparent anti-coop

77 ed transcription of a reporter driven by the HIV-1 LTR.

78 hibition of gene expression regulated by the HIV-1 LTR.

79 PMN-macrophage contact derepresses the HIV-1 LTR and enhances HIV-1 replication in alveolar mac

80 ubstituted for PMN contact, derepressing the HIV-1 LTR.

81 hibitory C/EBPbeta, thereby derepressing the HIV-1 LTR.

82 es activate NF-kappaB, further enhancing the HIV-1 LTR.

83 ion between ICP0 and Tat is specific for the HIV-1 LTR and was not observed with other promoters (e.g

84 roteins to activate gene expression from the HIV-1 LTR and found that KSHV ORF45 is the most potent a

85 lins DE and E repress transcription from the HIV-1 LTR and gene expression from the viral genome, rai

86 stimulates transcription elongation from the HIV-1 LTR and provides an important in vitro model syste

87 he transactivation of transcription from the HIV-1 LTR by binding to the transactivation response (TA

88 neurin is able to induce expression from the HIV-1 LTR in a p53- and NF-kappaB-dependent manner and P

89 s that could activate transcription from the HIV-1 LTR in an NF-kappaB-independent manner, and isolat

90 or that potently induces expression from the HIV-1 LTR in coinfected cluster of differentiation 4-pos

91 is able to stimulate transcription from the HIV-1 LTR promoter by activating NF-kappaB through a mec

92 imulates transcriptional elongation from the HIV-1 LTR.

93 in vitro transcriptional elongation from the HIV-1 LTR.

94 However, the HIV-1 LTR was not maximally stimulated and NF-kappaB was

95 g by human RNA polymerase II (RNAPII) in the HIV-1 LTR is caused principally by a weak RNA:DNA hybrid

96 The NFkappaB sites in the HIV-1 LTR were required for a response to cytokines but

97 these elements functionally inactivated the HIV-1 LTR when it was constrained in a chromatin configu

98 port the hypothesis that HCMV can induce the HIV-1 LTR when HIV-1 gene expression is minimal and that

99 s disclose the possibility of inhibiting the HIV-1 LTR promoter by G-quadruplex-interacting small mol

100 myristate acetate-induced activation of the HIV-1 LTR and activate the signal transducer and activat

101 lA bound to the tandem kappaB element of the HIV-1 LTR as a dimeric dimer, providing direct structura

102 AR and duplicated kappaB cis elements of the HIV-1 LTR as well as the NF-kappaB activation domain of

103 factors, thereby permitting induction of the HIV-1 LTR by both protein kinase C and A activation sign

104 that demonstrate that the regulation of the HIV-1 LTR by CA150 has the same functional requirements

105 hanism for transcriptional repression of the HIV-1 LTR by E1A 243R that is enhancer-independent and t

106 Activation of the HIV-1 LTR by HIC in NIH 3T3 cells occurs at the RNA leve

107 ibitor, SB203580, inhibits activation of the HIV-1 LTR by interleukin-1, tumor necrosis factor, UV li

108 e a novel role for PU.1 in activation of the HIV-1 LTR by LPS.

109 ese findings indicate that activation of the HIV-1 LTR in Jurkat T cells can be induced by H2O2 relea

110 onal studies revealed that activation of the HIV-1 LTR in LPS-stimulated cells requires both NF-kappa

111 CAF reconstituted Tat transactivation of the HIV-1 LTR in NIH3T3 cells to a level similar to that obs

112 ion, is important for T(3) regulation of the HIV-1 LTR in vivo.

113 e entirely dispensable for activation of the HIV-1 LTR promoter when CycT1/P-TEFb is artificially rec

114 arkably potent and specific inhibitor of the HIV-1 LTR promoter.

115 Repression of the HIV-1 LTR required intact CCAAT/enhancer binding protein

116 recruitment of TBP, while activation of the HIV-1 LTR requires steps in addition to TBP recruitment.

117 Extensive mutagenesis of the HIV-1 LTR revealed that PU.1-dependent activation requir

118 t region (MAR) present within the NRE of the HIV-1 LTR that recognizes a sequence-specific DNA-bindin

119 ne cell defect in Tat transactivation of the HIV-1 LTR was linked to the reduced abundance of p300 an

120 lized between nucleotides -51 and +12 of the HIV-1 LTR within the core promoter.

121 lin T1 enhanced not only the activity of the HIV-1 LTR, but also the glucocorticoid receptor-mediated

122 that recognizes the initiation region of the HIV-1 LTR.

123 EFb and increased Tat transactivation of the HIV-1 LTR.

124 enhances the transcriptional activity of the HIV-1 LTR.

125 s a further deletion in the U3 region of the HIV-1 LTR.

126 c arrangement of the two kappaB sites on the HIV-1 LTR can modulate the assembly kinetics of the high

127 ages induced depletion of HDAC1 and 3 on the HIV-1 LTR that was associated with hyperacetylation of h

128 utable to enhanced function of P-TEFb on the HIV-1 LTR.

129 ted with hyperacetylation of histones on the HIV-1 LTR.

130 part of their Tat coactivator effect on the HIV-1 LTR.

131 with NF-kappaB1 for its binding sites on the HIV-1 LTR.

132 CP0 stimulates transcription of not only the HIV-1 LTR but also the TAR-defective HIV-1 provirus.

133 This finding suggests that the HIV-1 LTR can negatively influence the internal CMV prom

134 ults are consistent with the notion that the HIV-1 LTR possesses functional redundancy which allows i

135 ed neurons in the brain, indicating that the HIV-1 LTR promoter is transcriptionally active in neuron

136 ted RNA Pol II were rapidly recruited to the HIV-1 LTR after NF-kappaB induction; however, these elon

137 -domain-containing protein that binds to the HIV-1 LTR and associates with the HIV-1 transactivator p

138 sought to further detail LSF binding to the HIV-1 LTR and factors that regulate LSF occupancy.

139 his phenomenon is unlikely restricted to the HIV-1 LTR but probably represents a general mechanism fo

140 monstrate that the DNA binding of p53 to the HIV-1 LTR can be modulated by calcineurin and provide a

141 NA polymerase II (Pol II) recruitment to the HIV-1 LTR closely mirrored RelA binding.

142 While NF-kappaB binding to the HIV-1 LTR induces serial waves of efficient RNA Pol II i

143 rate that recruitment of CycT1/P-TEFb to the HIV-1 LTR is fully sufficient to activate this promoter

144 tethering p160 coactivator molecules to the HIV-1 LTR, allowing full activation of this promoter by

145 By contrast, TBP recruitment to the HIV-1 LTR, although necessary for conferring Tat respons

146 ease in RNA polymerase II recruitment to the HIV-1 LTR, leading to enhanced transcriptional output.

147 it an elongation-competent polymerase to the HIV-1 LTR, the B cell-specific immunoglobulin heavy chai

148 ot demonstrate direct binding of PU.1 to the HIV-1 LTR, they illustrate a novel role for PU.1 in acti

149 cts in recruitment of PCAF and P-TEFb to the HIV-1 LTR.

150 titute a Tat/TAR-independent activity to the HIV-1 LTR.

151 a specific and regulated activity toward the HIV-1 LTR promoter, which is mediated by G-quadruplexes.

152 NA alone was sufficient to transactivate the HIV-1 LTR in BJAB cells.

153 ound that LANA was able to transactivate the HIV-1 LTR in the human B-cell line BJAB, human monocytic

154 or c-Jun synergistically transactivated the HIV-1 LTR through the NF-kappaB sites.

155 plex that synergistically transactivates the HIV-1 LTR.

156 signed to target a 34-bp sequence within the HIV-1 LTR (loxLTR).

157 ctive targeting of the U5 and U3 ends of the HIV-1 LTRs can inhibit IN function.

158 chanism(s) underlying transactivation of the HIV-1-LTR in these cells.

159 promoters, including the cdc2 promoter, the HIV-1-LTR, and the simian virus 40 minimal promoter.

160 Thus, HIV-1 LTR ATF/CREB binding site sequence variation may m

161 ered, FoxP3 enhances NFkappaB-p65 binding to HIV-1 LTR.

162 hat the nuclear corepressor NCoR is bound to HIV-1 LTR in unstimulated macrophages and is released fr

163 into target SupT1 lymphoblastoid cells under HIV-1 LTR transcriptional regulation via a retroviral-me

164 ivation of integrated, but not unintegrated, HIV-1 LTR.

165 driven luciferase expression correlated with HIV-1 LTR transcription, as measured by ribonuclease pro

166 In transient transfection studies with HIV-1 LTR-reporter gene constructs we found that pretrea