Figure 6.
Figure 6. ChIP analysis of human γ and β promoters in bone marrow and 11.5-dpc fetal liver cells. Chromatin from ln2 and human bone marrow cells was immunoprecipitated with antiacetylated H3 (AcH3) or H4 (AcH4) Abs. Immunoprecipitated and input samples were subjected to duplex PCR analysis with one primer set specific for huγ or huβ promoters and another specific for ZFP37 (mouse) or pax6 (human) gene. (A) ChIP analysis of huγ promoters in ln2 and human bone marrow HPCs and erythroid cells. (B) ChIP analysis of huγ and huβ promoters (tg-huγ and tg-huβ) in ln2 11.5-dpc fetal liver HPCs and erythroid cells. (C) ChIP and S1 nuclease protection assays of tg-huβ and tg-huγ promoters in ln2 TSA-treated Ter119+ cells. ChIP assays were performed with anti-AcH3 Abs, and the level of acetylation of TSA-treated samples (TSA) relative to their respective ethanol-treated (ETOH) controls is represented by bars with their corresponding SEM deviations. Mouse β-actin transcript was used as internal control for S1 nuclease protection assay; tg-huβ and tg-huγ expression level in TSA-treated cells is relative to the ethanol treated controls.

ChIP analysis of human γ and β promoters in bone marrow and 11.5-dpc fetal liver cells. Chromatin from ln2 and human bone marrow cells was immunoprecipitated with antiacetylated H3 (AcH3) or H4 (AcH4) Abs. Immunoprecipitated and input samples were subjected to duplex PCR analysis with one primer set specific for huγ or huβ promoters and another specific for ZFP37 (mouse) or pax6 (human) gene. (A) ChIP analysis of huγ promoters in ln2 and human bone marrow HPCs and erythroid cells. (B) ChIP analysis of huγ and huβ promoters (tg-huγ and tg-huβ) in ln2 11.5-dpc fetal liver HPCs and erythroid cells. (C) ChIP and S1 nuclease protection assays of tg-huβ and tg-huγ promoters in ln2 TSA-treated Ter119+ cells. ChIP assays were performed with anti-AcH3 Abs, and the level of acetylation of TSA-treated samples (TSA) relative to their respective ethanol-treated (ETOH) controls is represented by bars with their corresponding SEM deviations. Mouse β-actin transcript was used as internal control for S1 nuclease protection assay; tg-huβ and tg-huγ expression level in TSA-treated cells is relative to the ethanol treated controls.

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