Tat inhibition by didehydro-Cortistatin A promotes heterochromatin formation at the HIV-1 long terminal repeat.

ABSTRACT:

Background

Transcription from the integrated HIV-1 promoter is directly governed by its chromatin environment, and the nucleosome-1 downstream from the transcription start site directly impedes transcription from the HIV-1 promoter. The HIV-1 Tat protein regulates the passage from viral latency to active transcription by binding to the viral mRNA hairpin (TAR) and recruiting transcriptional factors to promote transcriptional elongation. The Tat inhibitor didehydro-Cortistatin A (dCA) inhibits transcription and overtime, the lack of low-grade transcriptional events, triggers epigenetic changes at the latent loci that "lock" HIV transcription in a latent state.

Results

Here we investigated those epigenetic changes using multiple cell line models of HIV-1 latency and active tra

SUBMITTER: Li C 

PROVIDER: S-EPMC6466689 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature