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. 2015 Dec 11;5:18100. doi: 10.1038/srep18100

Figure 2. ChIP-QPCR for histone modifications (H3K4me1 and H3K27ac) in human liver cancer cell (LC control) and normal liver cell (CC control).

Figure 2

(A) Schematic representation of one human rDNA repeat. The positions of QPCR amplicons in ChIP assays are indicated with solid bars. (B) Enrichment of H3K4me1 on rDNA analyzed by ChIP-QPCR. Chromatin from HepG2 cells was cross-linked and immunoprecipitated with H3K4me1 antibody, DNA was analyzed by QPCR with different sets of primers indicated in (A). The percentage of DNA associated with anti-H3K4me1 antibody was calculated relative to the DNA from ChIP input. Values are represented by means ± SD derived from three independent ChIP experiments, each experiment was tested by at least three independent QPCR reactions. Student’s t-test was performed between human liver cancer cell (LC Control) and normal liver cell (CC Control). (C) Enrichment of H3K27ac on rDNA analyzed by ChIP-QPCR. Chromatin from HepG2 cells was cross-linked and immunoprecipitated with H3K27ac antibody, DNA was analyzed by QPCR with different sets of primers indicated in (A). The percentage of DNA associated with anti-H3K27ac antibody was calculated relative to the DNA from ChIP input. Values are represented by means ± SD from three independent ChIP experiments, each experiment was tested by at least three independent QPCR reactions. Student’s t-test was performed between human liver cancer cell (LC Control) and normal liver cell (CC Control).