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editorial

. 2019 Jul 24;10(12):861–863. doi: 10.1007/s13238-019-0652-x

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© The Author(s) 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.

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Non-canonical substrates of FBXW7. 1) FBXW7 binds to XRCC4 and promotes its polyubiquitylation via the K63 linkage, not for degradation, but for facilitating Ku70/80 recruitment to enhance the NHEJ repair; 2) FBXW7 promotes γ-catenin polyubiquitylation via the K63 linkage to increase the transcriptional expression of 14-3-3σ, and to enhance the activity in growth suppression and G2/M arrest; 3) LSD1, a pseudo-substrate of FBXW7, destabilizes FBXW7 by disrupting its dimerization and triggering its self-ubiquitylation for degradation via both proteasome and lysosome pathways