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. 2021 Aug 10;5:75. doi: 10.1038/s41698-021-00215-x

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© The Author(s) 2021

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. 1 — a Three biological replicates of ATF7IP-JAK2 Ba/F3 cells were treated with a rux dose escalation for 3 months until resistance to the clinically relevant dose of 1 µM rux was achieved. Each of the three rux-resistant (RuxR) ATF7IP-JAK2 Ba/F3 cells acquired independent resistance to rux. Concurrently, ATF7IP-JAK2 Ba/F3 cells were cultured without treatment (Naïve) or treated with vehicle control (0.1% DMSO) to generate control cell lines. b Representative diagram of the ATF7IP-JAK2 fusion gene indicating localization of acquired point mutations within the JAK2 kinase domain. Annotations were made using the NCBI reference sequences for JAK2 variant 1 (NM_004972.4) and ATF7IP (NM_181352.2).