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. 2022 Apr 26;13:2242. doi: 10.1038/s41467-022-30026-y

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© The Author(s) 2022

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. 7 — CRL^KLHL20 catalyzes SERINC5 polyubiquitination at the TGN and produces K33/K48-brached chains at K130 of SERINC5. The K33-linked Ub chain (Ub-K33) potentiates SERINC5 trafficking to the plasma membrane, where it is packaged into HIV-1 virions to inhibit viral infection in the absence of Nef. However, when Nef is expressed, this viral accessory protein recruits CycK/CDK13 to phosphorylate the ICL4 of SERINC5. This phosphorylation triggers SERINC5 conformational change, resulting in recruitment of the AP2 complex to SERINC5 via Nef. SERINC5 is then targeted to the endocytic pathway and degraded in lysosomes via the K48-linked Ub chain (Ub-K48). BioRender was used for making the model.