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. 2015 Jan 21;6(9):7123–7135. doi: 10.18632/oncotarget.3344

Figure 3. HDAC2 influences NF-κB-dependent TP53 expression and p53 crosstalks with NF-κB to regulate NF-κB transcriptional activities.

Figure 3

(A) qPCR of TP53 in RKO cells stably transfected as indicated and additional knockdown of p65. Diminishing p65 abrogates enhanced TP53 expression. (B) ABCD assay showing p53 binding to NF-κB complexes using RKO cells stably transfected with HDAC2-V5, HDAC2K462R-V5 or GFP for control. The amount of p53 recruited to κB consensus sites is dependent on the HDAC2 status. More p53 is recruited to NF-κB when wild-type HDAC2 is present. (C) p53 knockdown attenuates the induction of NF-κB reporter gene by HDAC2; n=5.