In this study we provide evidence that the transcription factor BCL11B represses expression from the HIV-1 long terminal repeat (LTR) in T lymphocytes through direct association with the HIV-1 LTR. We also demonstrate that the NuRD corepressor complex mediates BCL11B transcriptional repression of the HIV-1 LTR. In addition, BCL11B and the NuRD complex repressed TAT-mediated transactivation of the HIV-1 LTR in T lymphocytes, pointing to a potential role in initiation of silencing. In support of all the above results, we demonstrate that BCL11B affects HIV-1 replication and virus production, most likely by blocking LTR transcriptional activity. BCL11B showed specific repression for the HIV-1 LTR sequences isolated from seven different HIV-1 subtypes, demonstrating that it is a general transcriptional repressor for all LTRs.
We formulate a mathematical model to investigate the
Dynamic properties of histone modification patterns. We then illustrate that
Our modeling framework can be used to capture key features of experimentally
Observed combinatorial chromatin states....
Few interventions have targeted clients of female sex workers in Central America, despite their potential role in HIV/STI prevention. Semi-structured interviews were conducted with 30 clients of female sex workers on attitudes towards prevention of HIV/STIs, barriers to condom use an...
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