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. 2021 Jul 8;21:789. doi: 10.1186/s12885-021-08479-z

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — The phosphoproteome analysis of K562 perturbed with Nilotinib. A Barplot represents the number of quantified PS in every replicate before imputation for K562 exposed to control (CTRL, red) or 1′000 nM Nilotinib (DRG, green) conditions. (B, C) Inhibition of ABL1 substrates with most abundant inhibition of the reference site pCRKL Y207 as shown by WB and MS (light green). The original western blots can be found in the additional file 2. D KAEA waterfall plot showing overactive (red) and underactive kinases (blue) after exposure of K562 to Nilotinib. E STRING kinase-signaling network of significantly positive (red) and negative (blue) enriched kinases. The magenta edged kinases with asterisks (*) highlight experimentally validated targets of Nilotinib. TS: tumor suppressor