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. 2022 Mar 1;13:1100. doi: 10.1038/s41467-022-28705-x

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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. 7 — UHMK1 was genetically inactivated in A375 cells using CRISPR-Cas9, and the MSCV-GFP vector was stably expressed in A375-Cas9 and A375-UHMK1-gRNA cells. UHMK1-V5, UHMK1-K54R-V5, and UHMK1-RNP1-mut-V5 (R369A-G370A-Q-V-F372A) were ectopically expressed in A375-UHMK1-gRNA cells. a RNA immunoprecipitation (RNA-IP) assays were performed in the indicated cell lines following treatment with DMSO or 1 μM Vem for 48 hr. The indicated mRNA transcripts were then analysed using RT-qPCR. Data represent mean ± SEM of n = 3 biologically independent experiments. b Sensitivity to Vem was assessed using dose-response assays and 50% growth inhibition (GI50) drug concentrations were calculated. Data represent mean ± SEM of n = 3 biologically independent experiments. Statistical significance was determined using a one-way ANOVA adjusted for multiple comparisons. Source data are provided as a Source Data file.