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. Author manuscript; available in PMC: 2013 Aug 17.
Published in final edited form as: Cell. 2012 Aug 17;150(4):685–696. doi: 10.1016/j.cell.2012.07.018

Figure 3. PKM2-Dependent H3-T11 Phosphorylation Promotes the Disassociation of HDAC3 from CCND1 and MYC Promoter.

Figure 3

Please also see supplemental Figure S5C.

Immunoblotting analyses were performed with the indicated antibodies.

(A, B) WT rH3 or rH3-T11A expression was reconstituted in endogenous H3-depleted U87/EGFR cells (A), which were then treated with or without EGF (100 ng/ml) for 6 h. ChIP analyses with a HDAC3 antibody were performed (B).

(C) GST-HDAC3 pull-down assay was performed by incubation of 100 ng of purified recombinant His-tagged WT histone H3 or H3-T11A mutant with or without immobilized GST-HDAC3, which was followed by incubation with 200 ng of purified recombinant WT His-PKM2 or His-PKM2 K367M in the presence of PEP.