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. 2019 Dec 3;17:160. doi: 10.1186/s12964-019-0477-5

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 6 — MORC2 dimerization is enhanced in response to DNA damage. a HeLa cells were treated with 8 μM CPT for the indicated times. Lysates were subjected to cross-linking assays, followed by immunoblotting analysis with the indicated antibodies (upper panel). The expression levels of γH2AX in lysates without chemical cross-linking are shown as a control for CPT-induced DNA damage (bottom panel). b HEK293T cells were transfected with HA-MORC2 and HA-MORC2 ∆C82. After 48 h of transfection, total cellular lysates were subjected to cross-linking assay. Immunoblotting analysis was carried out with the indicated antibodies (upper panel). The expression levels of γH2AX in lysates without chemical cross-linking are shown as a control for CPT-induced DNA damage (bottom panel). c HeLa cells were treated with 20 ng/mL EGF for the indicated times and subjected to cross-linking assay (upper panel). The expression levels of phosphorylated EGFR (Y1068) in lysates without chemical cross-linking are shown as a control for the activation of downstream signaling by EGF (bottom panel). d HeLa cells were treated with 200 μM CoCl₂ for the indicated times and subjected to cross-linking assay (upper panel). The expression levels of hypoxia-inducible factor 1α (HIF1α) in lysates without chemical cross-linking are shown as a control for the activation of hypoxia signaling by CoCl₂ (bottom panel)