ArticleNature cell biology2013
Ubiquitylation-dependent localization of PLK1 in mitosis.
Article in Nature cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
74 citing papers in PubMed, 114 citations in OpenAlex.
- USP21-mediated deubiquitylation stimulates NuMA recruitment to the cell cortex to promote mitotic spindle orientation.Cell death and differentiation · 2026Article
- USP1 driven mitotic dysregulation and PLK1 stabilization confer Lenvatinib resistance in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- PLK1 overexpression as a dual-role biomarker and therapeutic vulnerability in pulmonary adenocarcinoma.PeerJ · 2026Article
- PLK1 stabilizes β-catenin to drive colorectal carcinogenesis through NFKB2-mediated transcriptional activation of USP2a and site-specific phosphorylation.Theranostics · 2026Article
- The kinesin motor Kif9 regulates centriolar satellite positioning during interphase.Current biology : CB · 2025Article
- Polo-like kinase 1 maintains transcription and chromosomal accessibility during mitosis.Molecular biology of the cell · 2025Article
- RAS/ERK signaling and PLK1: Coordinating developmental regulation and disease mechanisms.Current opinion in cell biology · 2025Review
- Cullin 3-mediated ubiquitination restricts enterovirus D68 replication and is counteracted by viral protease 3C.Journal of virology · 2025Article
- PLK1 in cancer therapy: a comprehensive review of immunomodulatory mechanisms and therapeutic opportunities.Frontiers in immunology · 2025Review
- PTEN-deficient, chromosomal instability colorectal cancer is hypersensitive to STAT3 inhibition.International journal of biological sciences · 2025Article
- Uncovering Cell Cycle Dysregulations and Associated Mechanisms in Cancer and Neurodegenerative Disorders: A Glimpse of Hope for Repurposed Drugs.Molecular neurobiology · 2024Review
- COLEC10 inhibits the stemness of hepatocellular carcinoma by suppressing the activity of β-catenin signaling.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- PLK1 phosphorylation of ZW10 guides accurate chromosome segregation in mitosis.Journal of molecular cell biology · 2024Article
- A conserved N-terminal motif of CUL3 contributes to assembly and E3 ligase activity of CRL3Nature communications · 2024Article
- Overexpression of KLHL22 correlates with poor prognosis in patients with triple-negative breast cancer.Translational cancer research · 2024Article
- A ubiquitin-based effector-to-inhibitor switch coordinates early brain, craniofacial, and skin development.Nature communications · 2023Article
- UBAP2L-dependent coupling of PLK1 localization and stability during mitosis.EMBO reports · 2023Article
- Emerging role of ubiquitination/deubiquitination modification of PD-1/PD-L1 in cancer immunotherapy.Genes & diseases · 2023Review
- Kelch-like proteins in the gastrointestinal tumors.Acta pharmacologica Sinica · 2023Review
- When Just One Phosphate Is One Too Many: The Multifaceted Interplay between Myc and Kinases.International journal of molecular sciences · 2023Review
14 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 6 institutions in 5 countries.
Funding
Abstract
Polo-like kinase 1 (PLK1) critically regulates mitosis through its dynamic localization to kinetochores, centrosomes and the midzone. The polo-box domain (PBD) and activity of PLK1 mediate its recruitment to mitotic structures, but the mechanisms regulating PLK1 dynamics remain poorly understood. Here, we identify PLK1 as a target of the cullin 3 (CUL3)-based E3 ubiquitin ligase, containing the BTB adaptor KLHL22, which regulates chromosome alignment and PLK1 kinetochore localization but not PLK1 stability. In the absence of KLHL22, PLK1 accumulates on kinetochores, resulting in activation of the spindle assembly checkpoint (SAC). CUL3-KLHL22 ubiquitylates Lys 492, located within the PBD, leading to PLK1 dissociation from kinetochore phosphoreceptors. Expression of a non-ubiquitylatable PLK1-K492R mutant phenocopies inactivation of CUL3-KLHL22. KLHL22 associates with the mitotic spindle and its interaction with PLK1 increases on chromosome bi-orientation. Our data suggest that CUL3-KLHL22-mediated ubiquitylation signals degradation-independent removal of PLK1 from kinetochores and SAC satisfaction, which are required for faithful mitosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.