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 nces the amount of Tat available to activate HIV-1 LTR, we hypothesize that acidifying endolysosomes

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

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

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

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

11 6 resulted in cooperative inhibition of both HIV-1 LTR-driven gene expression and HIV-1 replication.

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

13 tissue distribution and copies of subtype C HIV-1 LTR, gag, env DNA and RNA, and the relative mRNA l

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

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

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

17 e most effective at cleaving patient-derived HIV-1 LTRs from five patients.

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

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

20 Using U87MG astrocytoma cells expressing HIV-1 LTR-driven luciferase and primary human astrocytes

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

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

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

24 1168c (PPE17) can augment transcription from HIV-1 LTR in monocyte/macrophage cells.

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

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

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

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

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

30 of HIV-1 Tat from endolysosomes and induced HIV-1 LTR transactivation.

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

32 le for REV-ERB synthetic agonists to inhibit HIV-1 LTR promoter activity and viral replication, suppo

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

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

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

36 l treatment, potentially due to intermittent HIV-1 LTR activation.

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

38 electively recognize and stabilize the major HIV-1 LTR G4 possibly by fitting and binding through H-b

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

40 8, and LFA-1 inhibited PMN membrane-mediated HIV-1 LTR derepression.

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

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

43 virion production and enhanced Tat-mediated HIV-1 LTR promoter transactivation, along with stabiliza

44 ing endolysosome pH, as well as Tat-mediated HIV-1 LTR transactivation in U87MG cells stably integrat

45 ecause the effects of ML-SA1 on Tat-mediated HIV-1 LTR transactivation were blocked using pharmacolog

46 ed endolysosomes and restricted Tat-mediated HIV-1 LTR transactivation.

47 me leakage and attenuated HIV-1 Tat-mediated HIV-1 LTR transactivation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 be released in order for it to activate the HIV-1 LTR promoter and facilitate HIV-1 viral replicatio

77 However, to activate the HIV-1 LTR promoter and increase HIV-1 replication, HIV-1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 imulates transcriptional elongation from the HIV-1 LTR.

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

110 to the two NF-kB binding sites found in the HIV-1 LTR enhancer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 t two G4s, transcriptional regulators of the HIV-1 LTR promoter.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 plex that synergistically transactivates the HIV-1 LTR.

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

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

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

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

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

178 nteractions, in this work for the first time HIV-1 LTR model featuring repressed, intermediate, and a

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

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

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

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

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

184 vation in U87MG cells stably integrated with HIV-1 LTR luciferase reporter.

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