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. 2006 Dec 11;401(Pt 1):87–96. doi: 10.1042/BJ20061119

Figure 5. Effect of SAM or MTA treatment on protein binding to the human BHMT NF-κB sites in vivo.

Figure 5

HepG2 cells were treated with SAM (5 mM) or MTA (1 mM) for 12 h and the ChIP assay was used to assess nuclear binding of p50, p65 and HDAC3 (A), or HDAC1 and HDAC2 (B) to the NF-κB sites within the −313 to +2 region of the human BHMT in an endogenous chromatin configuration as described in the Materials and methods section. PCR products from amplification of the NF-κB sites following immunoprecipitation with antisera against p50 or p65 demonstrate that SAM and MTA treatment increased p50 and p65 binding to the human BHMT NF-κB sites (A). In addition, SAM and MTA also increased HDAC1, HDAC2 and HDAC3 binding to the SAM region (A, B). Input genomic DNA (gDNA input) was used as a positive control and a no antibody immunoprecipitation (no Ab) was used as a negative control.