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. 2019 Jul 24;47(17):9160–9179. doi: 10.1093/nar/gkz639

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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 Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — CTCF recruitment to DNA lesions requires its N-terminal or zinc-finger domain. (A) U2OS cells were transfected with GFP-tagged full-length CTCF and its truncation constructs (see Figure 1D, top), and were subjected to laser micro-irradiation for up to 180 s. (B) Recruitment of the indicated GFP-tagged CTCF proteins (green; see Figure 1D top) to double-strand breaks induced by mCherry-LacI-FokI (red) in the endogenous CTCF-depleted (siCTCF) or control (siCTL) FokI-U2OS cells. The ectopically complemented C-terminal domain of CTCF in CTCF knockdown cells (GFP-tagged C and ZF-C in siCTCF cells, right) is also recognized with an antibody to endogenous CTCF (blue); scale bar: 10 μm.