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. 2022 Apr 22;50(8):4500–4514. doi: 10.1093/nar/gkac259

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© The Author(s) 2022. 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-NonCommercial License (https://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 4. — Increase in γH2AX level at telomeres in H3.3 E31 mouse ES cells. (A) Immunostaining of TERF1 (red; marker for telomere) and γH2AX (green) showing increased γH2AX at telomeres (indicated by arrows) in both interphase and mitotic H3.3 E31 cells. Y chromosomes are indicated by arrowheads. Scale bars: 4 μm. (B) Percentages (mean ± SEM, n = 3, 16 nuclei were analysed in each experiment) of co-localized TERF1/γH2AX foci (TIF) are shown, and increased TIFs are found in H3.3 E31 and Kdm4b^–/– cells. (C) ChIP-qPCR analyses (mean ± SEM, n = 3) of γH2AX at telomeres and Foxp3 (a control gene) in H3.3 S31, A31 and E31 mouse ES cell lines. (B, C) P-values calculated using Student's t-test (** P< 0.05; * P< 0.1; ns, non-significant).