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. 2023 Jul 18;14:4297. doi: 10.1038/s41467-023-40086-3

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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 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. 4 — A Endogenous HCK interacted with autophagy proteins ATG2A and CBL in macrophage cell line Raw264.7 by IP/WB. B Overexpression of HCK inhibited autophagy flux as more LC3 HiBiT reporter remained. HCK knockdown promoted autophagy flux as less LC3 HiBiT reporter remained. C HCK KO could promote autophagy by increasing LC3II/LC3I and decrease P62 levels with and without 3-MA treatment in mice BMDM cells. Western blots (D) and quantification (E) showed phospho-PI3K and phospho-AKT decreased in HCK KO BMDMs. However, there were no significant differences for phospho-Erk1/2 and phospho-EGFR with HCK KO. F Effect of HCK KO was abrogated in autophagy inducing by PP242 treatment. Baf1: bafilomycin A1. 3-MA: 3-methyladenine. Source data are provided as a Source Data file.