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. Author manuscript; available in PMC: 2010 Sep 4.
Published in final edited form as: Cell. 2009 Aug 20;138(5):1019–1031. doi: 10.1016/j.cell.2009.06.049

Figure 5. Inhibition of HDAC activities leads to further increases of acetylation levels in active genes.

Figure 5

A. HDAC inhibitor treatment causes remarkable increases in histone acetylation in active genes. Resting T cells were treated with TSA and Butyrate and the distribution of H3K9ac and H4K16ac was analyzed using ChIP-Seq. The acetylation pattern of the CD4 locus is shown as custom tracks on the UCSC genome browser. TSA+Bu: the cells were treated with TSA and Butyrate.

B. Pol II is highly enriched in the promoter and downstream of TSSs of active genes. The profiles of Pol II binding surrounding TSSs are shown for active, intermediately active and silent genes.

C. HDAC6 II is highly enriched in the promoter and downstream of TSSs of active genes. The profiles of Pol II binding surrounding TSSs are shown for active, intermediately active and silent genes.

D. The most increase in H3K9 acetylation is detected in the promoter and downstream of TSSs of active genes. Act:0h, Act:2h, Sil:0h, and Sil:2h: the normalized acetylation levels of the active genes and silent genes with TSA treatment (2 hrs) or no treatment (0 hr).

E. The most increase in H4K16 acetylation is detected in the promoter and downstream of TSSs of active genes.