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

Figure 1.

Figure 1

Phosphorylation of crucial DNA damage response proteins by ATR in ATM-deficient cells. (A) ATM-proficient (1BR3) or ATM-deficient (AT5BIVA and AT22IJE-T) immortalized fibroblasts or primary human skin fibroblasts (HSFs), or primary AT fibroblasts (AT2052) were irradiated with γ-rays and the phosphorylation of DDR proteins was assayed after 1 h by Western blotting with phospho-specific antibodies as indicated. (B) The phosphorylation of DDR proteins in AT5BIVA cells irradiated with 8 Gy of γ-rays was assayed after pretreatment with increasing doses of wortmannin or (C) after short interfering RNA (siRNA)-mediated knockdown of ATR or DNA-PKcs. AT, ataxia telangiectasia; ATM, ataxia telangiectasia mutated; ATR, ataxia telangiectasia and Rad3 related; Chk, checkpoint kinase; DDR, DNA damage response; DNA-PKcs, DNA-dependent protein kinase catalytic subunit; KAP-1, KRAB associated protein 1; scr, scrambled; SMC1, structural maintainance of chromosomes 1; WT, wild type.