alexa Regulation of HIV-1 gene expression by histone acetylation and factor recruitment at the LTR promoter.


Immunotherapy: Open Access

Author(s): Lusic M, Marcello A, Cereseto A, Giacca M, Lusic M, Marcello A, Cereseto A, Giacca M, Lusic M, Marcello A, Cereseto A, Giacca M, Lusic M, Marcello A, Cereseto A, Giacca M

Abstract Share this page

Abstract In HIV-1 infected cells, the LTR promoter, once organized into chromatin, is transcriptionally inactive in the absence of stimulation. To examine the chromosomal events involved in transcriptional activation, we analyzed histone acetylation and factor recruitment at contiguous LTR regions by a quantitative chromatin immunoprecipitation assay. In chronically infected cells treated with a phorbol ester, we found that acetylation of both histones H3 and H4 occurs at discrete nucleosomal regions before the onset of viral mRNA transcription. Concomitantly, we observed the recruitment of known cellular acetyl-transferases to the promoter, including CBP, P/CAF and GCN5, as well as that of the p65 subunit of NF-kappa B. The specific contribution of the viral Tat transactivator was assayed in cells harboring the sole LTR. We again observed nucleosomal acetylation and the recruitment of specific co-factors to the viral LTR upon activation by either recombinant Tat or a phorbol ester. Strikingly, P/CAF was found associated with the promoter only in response to Tat. Taken together, these results contribute to the elucidation of the molecular events underlying HIV-1 transcriptional activation.
This article was published in EMBO J and referenced in Immunotherapy: Open Access

Relevant Expert PPTs

Relevant Speaker PPTs

Recommended Conferences

Relevant Topics

Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version