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. 2011 Aug 16;22(1):17–25. doi: 10.1111/j.1750-3639.2011.00507.x

Figure 5.

Figure 5

Chromatin immunoprecipitation confirms heterochromatinization of the RRP22 promoter in human glioma tissues. Shown are ΔCt values (antibody/input) for chromatin immunoprecipitation with antibodies against H3ac (associated with euchromatin) and H3K9me3 (associated with heterochromatin) as well as the H3ac/H3K9me3 ratios for three different non‐neoplastic brain tissues (NB1, 4, 5) and seven glioblastomas. The numbers correspond to: T1, GB239; T2, GB1060; T3, GB1061; T4, GB1062; T5, GB1063; T6, GB1064; T7, GB1065. Note that in non‐neoplastic brain tissues, the ratio between anti‐H3ac and anti‐H3K9me3 is invariably exceeding 1, indicating a prevailing euchromatic stage of the H3‐bound promoters. Three glioblastomas (T2, T3 and T4) show a shift toward a heterochromatinization of H3‐bound RRP22 promoter DNA (ratio H3ac/H3K9me3 <1, ▾). One of these three patients has a concomitant RRP22 hypermethylation, while the other two patients lack RRP22 methylation indicating that histone modifications together with promoter hypermethylation or alone contribute to the frequent transcriptional downregulation of RRP22 in human gliomas (color‐code for visualization of mRNA expression and methylation status is the same as introduced in Figure 1). Also shown is the allelic status on 1p and 19q, the mutational status of IDH1 and IDH2 as well as the p53 protein expression score for all seven glioblastomas.