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. 2023 Jun 22;6:660. doi: 10.1038/s42003-023-05045-0

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© The Author(s) 2023, corrected publication 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a CRISPR-Cas9 mediated AXL knockout in SKOV3 and HeyA8. b CRISPR-Cas9 mediated SAM68 knockout in HeyA8. c Immunoblot of HeyA8 SAM68 KO treated with R428 and Olaparib. d Immunoblot of AXL nuclear localisation upon AXL inhibition in HeyA8 SAM68 KO. Numbers below blots reflect protein band intensity normalised against respective control. e Combination treatment of R428 with ATR inhibitor BAY1895344 in pooled SAM68 KO cell lines and f single clone SAM68 KO cell lines. g Combination index of R428 and BAY1895344. h Dose reduction index of BAY1895344. F_a Fraction affected.