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1 ith the HIV Tat protein to transactivate the HIV long terminal repeat.
2 eases in transcriptional elongation from the HIV long terminal repeat.
3 ranscription factor in the regulation of the HIV long terminal repeat.
4 nced docking of Tat at the TAR region of the HIV long terminal repeat.
5 tion of NF-kappaB and its recruitment to the HIV-long terminal repeat.
6 or complex that is associated with repressed HIV long terminal repeats.
7 r host cellular factors to interact with the HIV long terminal repeats.
9 ion factor involved in the regulation of the HIV long terminal repeat and is selectively activated fo
10 n of restrictive chromatin structures at the HIV long terminal repeat and limiting P-TEFb levels cont
11 of TAK in transcriptional regulation of the HIV long terminal repeat comes from experiments using in
12 f HIV RNA; however, only a weak induction of HIV long terminal repeat-driven transcription, which was
13 y virus (HIV) Tat-induced transactivation of HIV long terminal repeat (HIV-LTR), we examined the effe
14 TLR4, and TLR9 mediate microbial Ag-induced HIV-long terminal repeat (HIV-LTR) trans-activation and
15 e of Toll-like receptor 2 (TLR2) and TLR9 in HIV-long terminal repeat (HIV-LTR) trans-activation and
17 ication and TAR-dependent transactivation of HIV-long terminal repeat indicates that this short seque
18 e level of transcriptional activation of the HIV long terminal repeat (LTR) and is mediated by both c
19 HIV-infected CD8 lymphocytes, we quantified HIV long terminal repeat (LTR) DNA in CD8+ CD4- and CD8b
20 -mediated gene expression has shown that the HIV long terminal repeat (LTR) from the viral isolate HI
21 the status of the elongation complex on the HIV long terminal repeat (LTR) in a repressed state is n
22 is a strong transcriptional repressor of the HIV long terminal repeat (LTR) in resting alveolar macro
23 ays, the ability of Tat to transactivate the HIV long terminal repeat (LTR) in the late differentiate
24 nding to the kappaB enhancer elements of the HIV long terminal repeat (LTR) in the maintenance of vir
25 B and the NF-kappaB cis-acting motifs of the HIV long terminal repeat (LTR) play in regulating HIV tr
26 tested the ability of vhs expressed from the HIV long terminal repeat (LTR) promoter to inhibit HIV r
27 siently transfected with wild type or mutant HIV long terminal repeat (LTR) reporter constructs were
28 ver, following the reduction in H3K27 at the HIV long terminal repeat (LTR), subsequent exposure to t
29 etaA148E, and PKCalpha, PKCalphaA25E, induce HIV long terminal repeat (LTR)-dependent transcription i
30 (CYLD), increases HIV infection by enhancing HIV long terminal repeat (LTR)-driven transcription via
31 astrocytomas transiently transfected with an HIV long terminal repeat (LTR)-luciferase reporter that
34 g sites of the human immunodeficiency virus (HIV) long terminal repeat (LTR) control multiple activat
35 ssion from the human immunodeficiency virus (HIV) long terminal repeat (LTR)-and from NF-kappaB-depen
37 lysis of receptor and coreceptor expression, HIV-long terminal repeat (LTR) transactivation, and tran
38 helial cells (HMEC) were transfected with an HIV-long terminal repeat (LTR)-luciferase construct and
39 terbred with transgenic NF-kappaB reporters (HIV-long terminal repeat/luciferase [HLL]), we found exa
40 vated Raf-1 in Jurkat T cells stimulated the HIV long terminal repeat promoter activity and significa
41 ecreased Tat-mediated transactivation of the HIV long terminal repeat region, and this functionality
42 the loss of transactivation activity for the HIV long terminal repeat still binds Egr-3 but can no lo
43 oth organisms induced transcription from the HIV long terminal repeat that was dependent on intact NF
45 nced HIV expression in T cells and activated HIV long-terminal-repeat transcription in U38 cells.
46 element in the human immunodeficiency virus (HIV) long terminal repeat, which is required for activat
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