ArticleMolecular biology of the cell2015
Efficient APC/C substrate degradation in cells undergoing mitotic exit depends on K11 ubiquitin linkages.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Methods to Study the Molecular Mechanism and Drive the Design of Protein Degraders.Chemical reviews · 2026Review
- The Molecular Toolbox for Linkage Type-Specific Analysis of Ubiquitin Signaling.Chembiochem : a European journal of chemical biology · 2025Review
- Cellular parameters shaping pathways of targeted protein degradation.Communications biology · 2025Review
- Ubiquitination detection techniques.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Revisiting degron motifs in human AURKA required for its targeting by APC/CLife science alliance · 2023Article
- Ubiquitin-modifying enzymes in Huntington's disease.Frontiers in molecular biosciences · 2023Review
- CDK4/6 inhibitors downregulate the ubiquitin-conjugating enzymes UBE2C/S/T involved in the ubiquitin-proteasome pathway in ER + breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- Regulating the regulator: a survey of mechanisms from transcription to translation controlling expression of mammalian cell cycle kinase Aurora A.Open biology · 2022Review
- The E3 ubiquitin ligase HECTD1 contributes to cell proliferation through an effect on mitosis.Scientific reports · 2022Article
- Ubiquitylation of cyclin C by HACE1 regulates cisplatin-associated sensitivity in gastric cancer.Clinical and translational medicine · 2022Article
- The APC/C targets the Cep152-Cep63 complex at the centrosome to regulate mitotic spindle assembly.Journal of cell science · 2022Article
- Huntingtin Ubiquitination Mechanisms and Novel Possible Therapies to Decrease the Toxic Effects of Mutated Huntingtin.Journal of personalized medicine · 2021Review
- Mitochondrial Aurora kinase A induces mitophagy by interacting with MAP1LC3 and Prohibitin 2.Life science alliance · 2021Article
- OTUD6A Is an Aurora Kinase A-Specific Deubiquitinase.International journal of molecular sciences · 2021Article
- Ubiquitination in Plant Meiosis: Recent Advances and High Throughput Methods.Frontiers in plant science · 2021Review
- Advances on Plant Ubiquitylome-From Mechanism to Application.International journal of molecular sciences · 2020Review
- AURKA destruction is decoupled from its activity at mitotic exit but is essential to suppress interphase activity.Journal of cell science · 2020Article
- Ubiquitin Linkage Specificity of Deubiquitinases Determines Cyclophilin Nuclear Localization and Degradation.iScience · 2020Article
- Expanding Role of Ubiquitin in Translational Control.International journal of molecular sciences · 2020Review
- Unanchored Ubiquitin Chains, Revisited.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The ubiquitin proteasome system (UPS) directs programmed destruction of key cellular regulators via posttranslational modification of its targets with polyubiquitin chains. These commonly contain Lys-48 (K48)-directed ubiquitin linkages, but chains containing atypical Lys-11 (K11) linkages also target substrates to the proteasome--for example, to regulate cell cycle progression. The ubiquitin ligase called the anaphase-promoting complex/cyclosome (APC/C) controls mitotic exit. In higher eukaryotes, the APC/C works with the E2 enzyme UBE2S to assemble K11 linkages in cells released from mitotic arrest, and these are proposed to constitute an improved proteolytic signal during exit from mitosis. We tested this idea by correlating quantitative measures of in vivo K11-specific ubiquitination of individual substrates, including Aurora kinases, with their degradation kinetics tracked at the single-cell level. All anaphase substrates tested by this methodology are stabilized by depletion of K11 linkages via UBE2S knockdown, even if the same substrates are significantly modified with K48-linked polyubiquitin. Specific examination of substrates depending on the APC/C coactivator Cdh1 for their degradation revealed Cdh1-dependent enrichment of K11 chains on these substrates, whereas other ubiquitin linkages on the same substrates added during mitotic exit were Cdh1-independent. Therefore we show that K11 linkages provide the APC/C with a means to regulate the rate of substrate degradation in a coactivator-specified manner.
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