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. 2019 Nov 28;48(3):1285–1300. doi: 10.1093/nar/gkz1114

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© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — CSB-RAD52 cascade contributes to the repair of ROS induced telomeric DSB. (A) Colony formation assays for U2OS CSB KO cells with RAD52 knockdown by siRNA transiently expressing KR-TRF1. (B) The intensity of GFP-XRCC1 foci after CSB or RAD52 knockdown by siRNA at 4h and 24h after light activation. (C) The clearance of γ-H2AX after RAD52 knockdown. (D) The recruitment of RAD52 to RFP/KR/FOK1-TRF1after light activation or transfection. (E) The recruitment of RAD52 to KR-TRF1 after treating with DRB (20 μM, 24 h) and α-amanitin (100 μg/ml, 2 h), TERRA knockdown by LNA, or overexpressed with HA-RNaseH WT, D210N mutant. (F) Telomere aberrations were found in U2OS and U2OS RAD52 KO cells with or without transiently expressing KR-TRF1. For (B), (C), (D) and (E), Mean values with SD from 50 cells in three independent experiments are given. P-value is calculated by unpaired t-test. ***P < 0.001.