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. 2021 Nov 7;16:63. doi: 10.1186/s13027-021-00402-2

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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. 5 — Silencing of UBE2D1 decreased the ubiquitination level of SMAD4. A UBE2D1 was identified to associate with metastasis and SMAD signaling pathways using GSEA. B Co-Ip assay was performed to detect the interaction between UBE2D1 and SMAD4. C The protein level of SMAD4 was measured after transduction with shUBE2D1 or overexpression lentivirus. D The ubiquitination level of SMAD4 was measured after transduction with shUBE2D1 lentivirus. E SMAD4 was detected after transduction with shUBE2D1 lentivirus upon treatment with 100 μg/ml CHX. F SMAD4 was detected after transduction with UBE2D1 overexpression lentivirus and/or 10 μM of MG132