Ed cells. Furthermore, TNF- stimulation led to the appearance of Sp1 and initiating RNAPII on the 5'LTR and additional enrichments of initiating and elongating RNAPII on the 3'LTR. These effects are most likely achieved through the activation of NF-B, which stimulates several steps of viral transcription including the PIC formation, transcription initiation and transcription elongation. Thus, our
T the level of gene expression act cooperatively to establish and maintain HIV latency. In conclusion, our study reveals that TI represents a key mechanism that antagonizes proviral gene expression to promote the latency of HIV. Furthermore, it demonstrates several means that could be used to counteract TI for reactivating latent HIV. Future mechanistic studies linking TI and other transcriptional
T the level of gene expression act cooperatively to establish and maintain HIV latency. In conclusion, our study reveals that TI represents a key mechanism that antagonizes proviral gene expression to promote the latency of HIV. Furthermore, it demonstrates several means that could be used to counteract TI for reactivating latent HIV. Future mechanistic studies linking TI and other transcriptional
T the level of gene expression act cooperatively to establish and maintain HIV latency. In conclusion, our study reveals that TI represents a key mechanism that antagonizes proviral gene expression to promote the latency of HIV. Furthermore, it demonstrates several means that could be used to counteract TI for reactivating latent HIV. Future mechanistic studies linking TI and other transcriptional
S we failed to detect any Sp1 at the PP5*/ 5'LTR junction or in the coding region of the HIV genome (Figure 5B, bars 1, 2, 5 and 6). Thus, the absence of Sp1 at the 5'LTR in untreated cells is a result of TI due to the actively transcribed PP5* gene. The finding that TNF- stimulation increased the levels of Sp1 not only at the 3' but also at the 5'LTR indicates that stimulating PIC assembly on the
Ed cells. Furthermore, TNF- stimulation led to the appearance of Sp1 and initiating RNAPII on the 5'LTR and additional enrichments of initiating and elongating RNAPII on the 3'LTR. These effects are most likely achieved through the activation of NF-B, which stimulates several steps of viral transcription including the PIC formation, transcription initiation and transcription elongation. Thus, our
Ed cells. Furthermore, TNF- stimulation led to the appearance of Sp1 and initiating RNAPII on the 5'LTR and additional enrichments of initiating and elongating RNAPII on the 3'LTR. These effects are most likely achieved through the activation of NF-B, which stimulates several steps of viral transcription including the PIC formation, transcription initiation and transcription elongation. Thus, our
Pelleted in a conical tube and washed with cold phosphate-buffered saline. Sonication and immunoprecipitation were performed using Chromatin Immunoprecipitation (ChIP) Assay Kit (Upstate) according to the manufacturer's instructions. Antibodies used are presented in Table S2. As negative control, normal rabbit or mouse serum (Sigma-Aldrich) was used. Appropriate primer pairs (Table S1) were used t