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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 1. — UCHL3 regulates RAD51 IRIF and HR. (A) A panel of DUBs was knocked down in U2OS cells, and cellular response to 1 μM olaparib was assayed using colony formation assay. Error bars represent SEM from three independent experiments. (B) UCHL3 was knocked out in U2OS cells by CRISPR, and Western blot was performed with the indicated antibodies. (C) The sensitivity of control and UCHL3 knockout U2OS cells to olaparib was assessed using colony formation assay. Error bars represent SEM from three independent experiments. (D) The HR-mediated DSB repair capacity of control (Ctrl) and UCHL3 knockout U2OS cells was assessed using a reporter system. Error bars represent SEM from three independent experiments. Statistical significance was determined by ANOVA. (**) P < 0.01. (E) Control or UCHL3 knockout U2OS cells were treated with ionizing radiation (IR), and focus formation of the indicated factors was detected by immunofluorescence. Representative images are shown in the top panel. Quantification of the percentage of cells displaying foci is shown in the bottom panel. Error bars represent SEM from three independent experiments. Statistical significance was determined by two-tailed Student's t-test. (**) P < 0.01.