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Fig. 5 | Epigenetics & Chromatin

Fig. 5

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

Fig. 5

Progressive epigenetic silencing of HIV expression by the TT at inhibitor dCA. a During active transcription, Tat recruit P-TEFb to TAR to boost the transition from transcription initiation to elongation. Nuc-1 downstream are characterized with activating epigenetic marks and poised for productive transcription by the recruitment of SWI/SNF chromatin remodeling complex (BAF180). b dCA binds to Tat and blocks the recruitment of P-TEFb to TAR, to inhibit the transition of transcription initiation to elongation. The repressive SWI/SNF chromatin remodeling complex (BAF250) accumulates on the HIV promoter, resulting in increased Nuc-1 occupancy and increased repressive epigenetic marks. c Overtime the treatment with dCA promotes the establishment of a closed chromatin state with limited RNA polymerase II (RNAP II) recruitment to the promoter. dCA-mediated silencing is refractory to reactivation by various LRAs

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