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. 2012 Mar 6;40(12):5378–5388. doi: 10.1093/nar/gks189

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© The Author(s) 2012. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — BML-210 inhibits MEF2-dependent recruitment of HDAC4 to the frataxin promoter. ChIP assays were performed with chromatin from HeLa cells transfected with FLAG-tagged HDAC4 and GFP and/or FLAG-tagged MEF2C. Drug-treated and control-treated chromatin were immunoprecipitated with anti-FLAG antibody and normal rabbit IgG as negative control, and precipitated genomic DNA was amplified with primers flanking the MEF2 site on the endogenous FXN promoter. (A) Co-transfection of HeLa cells with both MEF2C and HDAC4 resulted in enhanced enrichment of HDAC4 on the FXN promoter. (B) 6 h treatment with 10 µM BML-210 diminished the MEF2C-mediated enrichment of HDAC4 on the Frataxin promoter (P < 0.04). (C) The BML-210 treatment did not significantly affect the MEF2C enrichment on the FXN promoter. Lower panels are schematic interpretations of the ChIP data. FXNp: frataxin promoter (magenta line); MEF2 dimer (blue triangles); HDAC4 (green bar); BML-210 (red triangle).