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Fig. 5 | Breast Cancer Research

Fig. 5

From: Ribosomal S6 kinase (RSK) plays a critical role in DNA damage response via the phosphorylation of histone lysine demethylase KDM4B

Fig. 5

Effects of phospho-site mutations on KDM4B function in response to DNA damage. (A) Parental WT or KDM4B-KO MCF-7 and T-47D cells, or KDM4B-KO cells add-backed with WT or S666A/D mutant KDM4B, were cultured with or without Dox and subjected to immunoblotting with the indicated antibodies. (B and C) Parental T-47D or KDM4B-KO cells expressing exogenous KDM4B as indicated (B) or KDM4B-KO cells expressing S666D mutant incubated with or without BI-D1870 (C) were laser microirradiated followed by immunofluorescence analysis as in Fig. 1A. The relative intensities of KDM4B are shown with means and SDs in the right panels. ***P < 0.0001. N.S., not significant. (D and E) Either WT or KDM4B-S666D T-47D (D) and MCF-7 cells (E) were incubated with the indicated RSK inhibitors and analyzed for the recovery of IR-induced γH2AX foci as in Fig. 1E and F. *P < 0.01, **P < 0.002, ***P < 0.0001

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