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. 2018 Sep 14;9:3744. doi: 10.1038/s41467-018-06275-1

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© The Author(s) 2018

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. 2 — Inhibition of autophagy results in Fn14 accumulation and redistribution into large vesicular structures. a–c Transfected cells as follows were treated with BafA and TWK as indicated and extracted proteins were immunoblotted: a HeLa cells were transfected with non-targeting siRNA (siNT) or siRNA against TSG101 (siTSG101); b WT and ATG5-knockout (atg5⁻^/–) MEFs were transfected with overexpression plasmid of Flag-Fn14; c HeLa cells transfected with siNT or siRNA against ATG7 and ATG3 (siATG7 + 3). d–g HeLa cells as follows were treated with BafA and TWK as indicated, immunostained for Fn14, and analyzed by confocal microscopy (scale bar, 20 µm): d cells transfected with siNT or siRNA against all six Atg8 isoforms (siAtg8s); e WT or ATG4B^DN stable expression cells; f cells transfected with siNT or siRNA against BECN1 (siBECN1); g HeLa WT cells or CRISPR knockout of all Atg8s (HEXA)