Figure 5
Figure 5. Histone modification and regulatory polymorphism in VKORC1. (A) Relative amount of DNA fragments from different regions of the VKORC1 locus precipitated by antiacetyl-H3 and antitrimethyl-H3 antibodies in human liver samples. ChIP assays in frozen liver tissues were performed after micrococcal nuclease digestion, and precipitated DNA was recovered and quantified by real-time PCR. β2-microglobulin (B2M) serves as internal control. (B) Allele-specific DNA analysis after ChIP with antiacetyl-H3 and antitrimethyl-H3 in human livers, HepG2 cells, and B lymphocytes, using promoter SNP −1639G>A as a marker. The allelic DNA ratio from control DNA (no ChIP) was set as 1, and allelic DNA ratios from precipitates were normalized to the ratio of input. Data are means plus or minus SD (**P < .01, ***P < .001, compared with input ratio, ANOVA with Dunnett posttest).

Histone modification and regulatory polymorphism in VKORC1. (A) Relative amount of DNA fragments from different regions of the VKORC1 locus precipitated by antiacetyl-H3 and antitrimethyl-H3 antibodies in human liver samples. ChIP assays in frozen liver tissues were performed after micrococcal nuclease digestion, and precipitated DNA was recovered and quantified by real-time PCR. β2-microglobulin (B2M) serves as internal control. (B) Allele-specific DNA analysis after ChIP with antiacetyl-H3 and antitrimethyl-H3 in human livers, HepG2 cells, and B lymphocytes, using promoter SNP −1639G>A as a marker. The allelic DNA ratio from control DNA (no ChIP) was set as 1, and allelic DNA ratios from precipitates were normalized to the ratio of input. Data are means plus or minus SD (**P < .01, ***P < .001, compared with input ratio, ANOVA with Dunnett posttest).

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