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. 2021 Apr 1;106(4):1188–1192. doi: 10.3324/haematol.2020.259275

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Copyright© 2021 Ferrata Storti Foundation

This article is distributed under the terms of the Creative Commons Attribution Noncommercial License (by-nc 4.0) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.

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Figure 3. — UBE2T does not have a major role in the repair of non-interstrand crosslink DNA lesions. (A) Cell survival assay after ultraviolet treatment of complemented pairs of RA2627 fibroblasts compared to BJ wild-type (WT) fibroblasts depleted of XPF used as a positive control. The immunoblot shows decreased XPF levels after siRNA depletion. (B) Cell survival assay of RA2627 fibroblasts after treatment with irradiation. HA239F fibroblasts with RAD50 mutations are sensitive to irradiation and act as a positive control (RAD50^mut). (C, D) Cell sensitivity assays comparing RA2627 fibroblasts to RA3331 Fanconi anemia patient-derived fibroblasts with SLX4 mutations (SLX4^mut) expressing WT SLX4 or empty vector exposed to camptothecin (C) and the PARP inhibitor, olaparib (D). (E) Cell survival assay after hydroxyurea treatment of RA2627 cells compared to the RA3226 BRCA2 patient cell line (BRCA2^mut). Error bars indicate the standard deviation. EV: empty vector; UV: ultraviolet irradiation; IR: irradiation; CPT: camptothecin; PARPi: PARP inhibitor; HU: hydroxyurea.