ArticleNature cell biology2015
Degradation of Cep68 and PCNT cleavage mediate Cep215 removal from the PCM to allow centriole separation, disengagement and licensing.
Article in Nature cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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
55 citing papers in PubMed, 86 citations in OpenAlex.
- Article
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- Centrosome-Signaling Pathway Crosstalk: A Core Hub From Cellular Homeostasis to Disease.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Centrosome linker protein CEP68 modulates cellular stress responses via nuclear condensate formation and HSP27 interaction.iScience · 2026Article
- Critical constituents and assembly principles of centriole biogenesis in human cells.Nature reviews. Molecular cell biology · 2026Review
- NuSAP Safeguards Centriole Integrity to Mediate CEP57-CEP152 Torus Recruitment for Proper Engagement.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Atrial Fibrillation and Primary Cilia-Associated Genes: The Role of CEP68.International journal of molecular sciences · 2026Article
- Crosstalk between the circadian clock, intestinal stem cell niche, and epithelial cell fate decision.Genes & diseases · 2025Review
- 14-3-3ε inhibits premature centriole disengagement by inhibiting the activity of Plk1 and separase.Journal of cell science · 2025Article
- SKP1-CUL1-F-box: Key molecular targets affecting disease progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- PPTC7 antagonizes mitophagy by promoting BNIP3 and NIX degradation via SCFEMBO reports · 2024Article
- Mild replication stress causes premature centriole disengagement via a sub-critical Plk1 activity under the control of ATR-Chk1.Nature communications · 2023Article
- Genetic Primary Microcephalies: When Centrosome Dysfunction Dictates Brain and Body Size.Cells · 2023Review
- FBXL4 suppresses mitophagy by restricting the accumulation of NIX and BNIP3 mitophagy receptors.The EMBO journal · 2023Article
- Review
- Pathogenic LRRK2 regulates centrosome cohesion via Rab10/RILPL1-mediated CDK5RAP2 displacement.iScience · 2022Article
- Homozygous mutation inJournal of medical genetics · 2022Article
- Role of Polo-like Kinases Plk1 and Plk4 in the Initiation of Centriole Duplication-Impact on Cancer.Cells · 2022Review
- Triple deletion ofCell cycle (Georgetown, Tex.) · 2021Article
- Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
An intercentrosomal linker keeps a cell's two centrosomes joined together until it is dissolved at the onset of mitosis. A second connection keeps daughter centrioles engaged to their mothers until they lose their orthogonal arrangement at the end of mitosis. Centriole disengagement is required to license centrioles for duplication. We show that the intercentrosomal linker protein Cep68 is degraded in prometaphase through the SCF(βTrCP) (Skp1-Cul1-F-box protein) ubiquitin ligase complex. Cep68 degradation is initiated by PLK1 phosphorylation of Cep68 on Ser 332, allowing recognition by βTrCP. We also found that Cep68 forms a complex with Cep215 (also known as Cdk5Rap2) and PCNT (also known as pericentrin), two PCM (pericentriolar material) proteins involved in centriole engagement. Cep68 and PCNT bind to different pools of Cep215. We propose that Cep68 degradation allows Cep215 removal from the peripheral PCM preventing centriole separation following disengagement, whereas PCNT cleavage mediates Cep215 removal from the core of the PCM to inhibit centriole disengagement and duplication.
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Registered trials
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.