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. 2023 Dec 18;20(1):28–55. doi: 10.1038/s44320-023-00004-7

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© The Author(s) 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

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Figure EV6 — (A) Experimental workflow and number of protein and phosphopeptide identifications/quantification. For each time point of drug treatment, a DMSO control was included to account for abundance changes that are not due to the drug treatment. (B) Number of drug-induced protein expression changes (left panel) and phosphopeptide abundance (at least twofold compared to zero min at different time points). (C) Heatmap of fold-changes of phosphopeptides from proteins involved in FGFR signalling (annotations from Reactome) compared to DMSO at different time points after Infigratinib treatment. (D) Time course of p-sites of MAST2 and ULK2 proteins following Infigratinib treatment. (E) Elastic net regression analysis using the phosphorylation site S1552 of TOP2B to identify drugs associated with this p-site. (F) TOP2B protein level at different time points after Infigratinib treatment. (G) Distribution of AUC values from the phenotypic drug screen in G401 cells (139 kinase inhibitors shown). Inhibitors targeting HER2 are highlighted in red. (H) Time course of EZH2 T487 following Infigratinib treatment.