Luded from the analysis.Nature. Author manuscript; available in PMC 2016 November 29.Gautam et al.PageAntibodiesAuthor Manuscript Author Manuscript Author Manuscript Author ManuscriptThe VRC01, 3BNC117, 10-1074 and VRC01-LS anti-HIV-1 monoclonal NAbs were isolated and produced as described elsewhere 9-12. 10-1074 was produced by transient transfection of IgH and IgL expression plasmids into the hu
K of the latent provirus in J-Lat 9.2 cells is TI of the 5'LTR caused by the transcription of the host PP5* gene. This interfering transcription results in the lack of Sp1 and the presence of the elongating RNAPII at the 5'LTR. Moreover, TI can be partially rescued by TNF- stimulation, as documented by the appearance of Sp1 and initiating RNAPII at the 5'LTR. The slight enrichment of the RNAPII in
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Ns dormant. In contrast, we demonstrated that TI could be counteracted by specific inhibition of the upstream transcription or by cooperative activation of transcription initiation and elongation from the 5'LTR by the viral and host TFs. In the latter scenario, we envision that RNAPII initiating from the viral promoter competes successfully with the RNAPII that is elongating through the 5'LTR. Bec
Mpared GFP expression of parental and J-Lat shER cells using fluorescence activated cell sorting (FACS). As expected, no GFP-expressing cells could be detected in untreated cells (Figures 6C-6F, mock). About 20 of cells turned GFP-positive in TNF--treated J-Lat 9.2 cells (Figure 6C, TNF-). Importantly, the inhibition of PP5 transcription synergized with TNF- to increase further the number of GFP-
Me transcription through the provirus, since slight enrichment of elongating RNAPII in the HIV coding region of transcriptionally silent J-Lat 9.2 cells was observed using ChIPqPCR assay. However, transcription originating from the host promoter, ignoring pA sites in both LTRs and consequently splicing out the provirus together with the host intron (Han et al., 2004) is most likely less frequent t
Me transcription through the provirus, since slight enrichment of elongating RNAPII in the HIV coding region of transcriptionally silent J-Lat 9.2 cells was observed using ChIPqPCR assay. However, transcription originating from the host promoter, ignoring pA sites in both LTRs and consequently splicing out the provirus together with the host intron (Han et al., 2004) is most likely less frequent t
Me transcription through the provirus, since slight enrichment of elongating RNAPII in the HIV coding region of transcriptionally silent J-Lat 9.2 cells was observed using ChIPqPCR assay. However, transcription originating from the host promoter, ignoring pA sites in both LTRs and consequently splicing out the provirus together with the host intron (Han et al., 2004) is most likely less frequent t