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. 2006 Sep;26(18):6748–6761. doi: 10.1128/MCB.00560-06

FIG. 8.

FIG. 8.

TSA causes release of p107 from the LHR gene promoter independently of histone acetylation status. (A) Immunoblotting analyses of the levels of acetylated histones H3 (AceH3) and H4 (AceH4) in TSA-treated or untreated JAR cells in the presence of different doses of the PKCζ inhibitor PS-PKCζ. The total H4 protein level is also shown. (B) Quantitative ChIP analyses of the association of acetylated H3 or H4 with the LHR gene promoter (left) and the human β-actin promoter (right) in JAR cells treated with or without TSA, PS-PKCζ, or both. (C) Quantitative ChIP analyses of the association of Sp1, HDAC1, HDAC2, mSin3A, pRb, and p107 with the LHR gene promoter (left) and the human β-actin promoter (right) in TSA-treated or untreated JAR cells. Results are expressed as percentages of the total input DNA.