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. 2016 Dec 1;30(23):2581–2595. doi: 10.1101/gad.289439.116

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© 2016 Luo et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 3. — UCHL3 regulates HR and radiosensitivity through RAD51. (A) The HR-mediated DSB repair capacity of control cells, UCHL3 knockout cells, and UCHL3 knockout cells stably expressing the indicated constructs was assessed using a reporter system. (B) The sensitivity of control cells, UCHL3 knockout cells, and UCHL3 knockout cells stably expressing the indicated constructs to IR was assessed using colony formation assay. (C) Control and UCHL3 knockout U2OS cells stably expressing control or RAD51 shRNA were subjected to HR assay. (D) The sensitivity of control cells and UCHL3 knockout U2OS cells stably expressing control or RAD51 shRNA to IR was assessed using colony formation assay. (A–D) Error bars represent SEM from three independent experiments. Statistical significance was determined by two-tailed Student's t-test, (*) P < 0.05; (**) P < 0.01; (n.s.) no significant difference.