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. 2015 Mar 26;43(9):4505–4516. doi: 10.1093/nar/gkv176

Figure 1.

Figure 1.

AKT phosphorylates H3–45 in response to DNA damage. (A) AKT substrate sequences conserved in various proteins, including histones H2B and H3. (B) Immunofluorescence staining of phosphorylated AKT-serine 473 (p-AKT-S473) and phosphorylated H3-threonine 45 (p-H3-T45) in MCF10A cells. Cells were treated with DMSO, 100 μM etoposide (ETPS), 0.4 μg/ml adriamycin (ADR) or 50 J/m2 UV irradiation (UV) for 18 h. DNA counterstained with DAPI; scale bar, 20 μm. (C) Western blot of samples in (B). (D) MCF10A cells were treated with DMSO, 0.4 μg/ml ADR, 0.2 μM AKT inhibitor IV (IV) or 0.4 μg/ml ADR and 0.2 μM AKT inhibitor IV for 18 h. Total cell extracts were probed by western blot. Data shown are the representative of three independent experiments.