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. 2020 Nov 4;10:19068. doi: 10.1038/s41598-020-76227-7

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© The Author(s) 2020

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/.

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PI4KIIIβ is involved in CVB3-induced LC3 lipidation. (A) Schematic diagram of the proposed role of PI4KIIIβ in autophagy and the known function in enterovirus replication. (B) PI4KIIIβ was transiently silenced in HEK293A cells using siRNA for 48 h. Cells were then subjected to sham or CVB3 infection for 16 h, followed by western blot analysis of LC3 and PI4KIIIβ. Densitometry was measured as above, and the results are presented underneath and in right panel (mean ± SD, n = 3. Analyzed by one way ANOVA with Tukey’s post-test). (C) HEK293A cells, transfected with control or PIK3C3, PI4KIIIβ, or PIKfyve siRNAs for 48 h, were sham- or CVB3-infected. Western blotting was performed for detection of LC3, VP1, PIK3C3, PI4KIIIβ, or PIKfyve, and quantified as above (right panel) (mean ± SD, n = 3. Analyzed by one way ANOVA with Tukey’s post-test). N.S. not significant.