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. Author manuscript; available in PMC: 2018 Nov 1.

Published in final edited form as: DNA Repair (Amst). 2013 Dec 15;13:22–31. doi: 10.1016/j.dnarep.2013.11.002

Fig. 2. — WT controls or A-T cells were submitted to treatment with 200 μM H₂O₂ for 60 min and allowed to recover for up to 48h. MtDNA integrity was analyzed using QPCR; data were normalized to mtDNA copy number. Experiments were reproduced at least 3 independent time; error bars reflect ± SEM. (A) Patient- derived fibroblasts GM07532 (WT) and GM02052 (A-T), (B) patient-derived cells AG01522 (WT) and AG04405 (A-T). (C) mtDNA repair kinetics was evaluated in GM07532 (WT) upon knock down of ATM using siRNA. (D) Kinetics of mtDNA repair was followed in GM07532 (WT) up to 24h after H₂O₂ exposure in the presence or absence of 1 μM triapine, a RR-inhibitor. NS = not-significant.

Fig. 2. — WT controls or A-T cells were submitted to treatment with 200 μM H₂O₂ for 60 min and allowed to recover for up to 48h. MtDNA integrity was analyzed using QPCR; data were normalized to mtDNA copy number. Experiments were reproduced at least 3 independent time; error bars reflect ± SEM. (A) Patient- derived fibroblasts GM07532 (WT) and GM02052 (A-T), (B) patient-derived cells AG01522 (WT) and AG04405 (A-T). (C) mtDNA repair kinetics was evaluated in GM07532 (WT) upon knock down of ATM using siRNA. (D) Kinetics of mtDNA repair was followed in GM07532 (WT) up to 24h after H₂O₂ exposure in the presence or absence of 1 μM triapine, a RR-inhibitor. NS = not-significant.