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. Author manuscript; available in PMC: 2011 May 11.
Published in final edited form as: J Biol Chem. 2005 Feb 24;280(17):17163–17171. doi: 10.1074/jbc.M501375200

Fig. 5. Recruitment of HDAC-1 at the silencer by SLUG is correlated with decrease in acetyl histones at the BRCA2 promoter.

Fig. 5

A, a ChIP assay showing the in vivo binding of SLUG, CtBP-1, and HDAC-1 at the silencer in the non-dividing MDA-MB-231 and BT-549 cells but not in the non-dividing MDA-MB-468 cells. There was no amplification of the silencer DNA in the transfection when no antibody or preimmune rabbit serum was used (data not shown). The lowest panel is an amplification of input DNA prior to immunoprecipitation. B, ChIP assay showing the levels of acetyl histones H3 and H4 at the BRCA2 promoter in BT-549 cells. Cells were treated without (−TSA) or with (+TSA) trichostatin A (100 nM) for 24 h before ChIP assay. The lowest panel is an amplification of input DNA prior to immunoprecipitation. There is no change in the amplification of input DNA in all the cases. C, functional evaluation of the activity of the BRCA2 gene silencer in non-dividing BT-549, MDA-MB-231, and MDA-MB-468 cells in the presence or absence of the HDAC inhibitor, trichostatin A (100 nM). Data are presented as mean ± S.E. All experiments were done six times in triplicate. The differences between the luciferase activities in the cells treated with the solvent dimethyl sulfoxide (DMSO) or trichostatin A were statistically significant (p < 0.0001). RLU, relative light units.