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. 2014 Apr 1;42(9):5594–5604. doi: 10.1093/nar/gku236

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© The Author(s) 2014. 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/3.0/), 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 1. — Activation of AMPK can suppress histone H2B O-GlcNAcylation. (A) AICAR treatment in MEFs for 12 h strongly inhibited histone H2B O-GlcNAcylation and H2B K120 monoubiquitination. (B) This effect in (A) by AICAR could be reversed by Compound C. (C) Histone H2B O-GlcNAcylation and H2B K120 monoubiquitination signals were examined in wild-type (WT) or AMPKα1- and AMPKα2-deficient MEFs (ampkα−/−) treated with or without AICAR. (D) The expression of histone H2B O-GlcNAcylation common target genes in (C) was analyzed by qRT-PCR. Data analysis is explained in the Materials and Methods section. All error bars denote s.d., n = 3.