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. 2001 Apr 17;98(9):4990–4995. doi: 10.1073/pnas.101617298

Figure 2.

Figure 2

ChIP analysis of the occupancy of p16 and p14 promoters by methyl-CpG binding proteins. (A) A quantitative analysis of PCR products was performed on chromatin immunoprecipitated with various amounts of antibodies against MBD2 and MeCP2 in HCT 15 cells. For the different conditions, the bound (B) and unbound (U) fractions were amplified with primers specific for p16, p14, and Alu. (B) Histograms of the ratio of the bound DNA fraction vs. the unbound DNA fraction normalized to the no antibody value (lane 6, p16; lane 12, p14; lane 15, Alu). Data are the mean ± SD for at least three experiments. (C) As a control experiment, amplification of the bound and unbound fractions was performed in HeLa where p16 and p14 are unmethylated. (D) DNA corresponding to the transcription start site of the BRCA1 gene was amplified with primers for exon 1a (16), after digestion of genomic DNA with HpaII or CfoI (lanes 8 and 9), or after ChIP, on input (lane 7), bound (lanes 1–6, Upper) and unbound (lanes 1–6, Lower) fractions.