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. 2009 May 15;10(6):629–635. doi: 10.1038/embor.2009.60

Figure 2.

Figure 2

Sequential recruitment of RPA and ATR to double-strand breaks in ATM-deficient cells. (A) 1BR3, 1BR3 pre-treated with KU55933 or AT5BIVA cells were laser micro-irradiated and co-immunofluorescence stained with γH2AX antibodies and either RPA antibodies (top panel) or ATR antibodies (bottom panel) at the indicated times. These cells were also co-immunofluorescence stained with RPA antibodies and ATR antibodies at 30 min. (B) 1BR3 or AT5BIVA cells were immunofluorescence stained as indicated 1 h after irradiation with 8 Gy of γ-rays. ATM, ataxia telangiectasia mutated; ATR, ataxia telangiectasia and Rad3 related; DAP1, 4′,6-diamino-2-phenylindole; γH2AX, phosphorylated H2AX; RPA, replication protein A.