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. 2015 May 15;43(12):5759–5770. doi: 10.1093/nar/gkv498

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© The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — H2A phosphorylation. (A) ChIP with DDY3 WT and corresponding hmo1Δ strain using antibody to phosphorylated H2A at MAT and at 29.5 kb upstream of DSB during DNA damage (galactose) and repair (glucose). IC, input control; No, no antibody; IP, immunoprecipitation with antibody to γ-H2AX. (B) Densitometric analysis of ChIP data shown in (A), obtained with ImageJ software. (C) ChIP with JKM179 WT and corresponding hmo1Δ strain using antibody to phosphorylated H2A at MAT and at 29.5 kb upstream of DSB during DNA damage (galactose) and repair (glucose). (D) Densitometric analysis of ChIP data shown in (C). Fold enrichment = ChIP/Input DNA. Three independent experiments were performed. Error bars represent standard deviation.