ArticleNature2001
Cdc6 cooperates with Sic1 and Hct1 to inactivate mitotic cyclin-dependent kinases.
Article in Nature, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 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
29 citing papers in PubMed, 88 citations in OpenAlex.
- CDC6 Inhibits CDK1 Activity in MII-Arrested Oocyte Cell-Free Extract.International journal of molecular sciences · 2025Article
- Ubiquitin protease Ubp1 cooperates with Ubp10 and Ubp12 to revert lysine-164 PCNA ubiquitylation at replication forks.Nucleic acids research · 2025Article
- Timely lagging strand maturation relies on Ubp10 deubiquitylase-mediated PCNA dissociation from replicating chromatin.Nature communications · 2024Article
- CDC6 as a Key Inhibitory Regulator of CDK1 Activation Dynamics and the Timing of Mitotic Entry and Progression.Biology · 2023Review
- An essential Noc3p dimerization cycle mediates ORC double-hexamer formation in replication licensing.Life science alliance · 2023Article
- The budding yeast GSK-3 homologue Mck1 is an essential component of the spindle position checkpoint.Open biology · 2022Article
- LncRNAs of Saccharomyces cerevisiae bypass the cell cycle arrest imposed by ethanol stress.PLoS computational biology · 2022Article
- Article
- DNA Replication Licensing Factors: Novel Targets for Cancer Therapy via Inhibiting the Stemness of Cancer Cells.International journal of biological sciences · 2022Review
- Cyclin-Specific Docking Mechanisms Reveal the Complexity of M-CDK Function in the Cell Cycle.Molecular cell · 2019Article
- Cell Division Cycle 6 Promotes Mitotic Slippage and Contributes to Drug Resistance in Paclitaxel-Treated Cancer Cells.PloS one · 2016Article
- A Model of Yeast Cell-Cycle Regulation Based on a Standard Component Modeling Strategy for Protein Regulatory Networks.PloS one · 2016Article
- Dynamics of ASXL1 mutation and other associated genetic alterations during disease progression in patients with primary myelodysplastic syndrome.Blood cancer journal · 2014Article
- Regulating DNA replication in eukarya.Cold Spring Harbor perspectives in biology · 2013Review
- Decoding ubiquitin for mitosis.Genes & cancer · 2012Article
- Reversal of PCNA ubiquitylation by Ubp10 in Saccharomyces cerevisiae.PLoS genetics · 2012Article
- Regulation of the final stage of mitosis by components of the pre-replicative complex and a polo kinase.Cell cycle (Georgetown, Tex.) · 2011Article
- Canonical and Alternative Pathways in Cyclin-Dependent Kinase 1/Cyclin B Inactivation upon M-Phase Exit in Xenopus laevis Cell-Free Extracts.Enzyme research · 2011Article
- Cell division cycle 6, a mitotic substrate of polo-like kinase 1, regulates chromosomal segregation mediated by cyclin-dependent kinase 1 and separase.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Deregulated Cdc6 inhibits DNA replication and suppresses Cdc7-mediated phosphorylation of Mcm2-7 complex.Nucleic acids research · 2010Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exit from mitosis requires the inactivation of mitotic cyclin-dependent kinases (CDKs). In the budding yeast, Saccharomyces cerevisiae, inactivation of CDKs during late mitosis involves degradation of B-type cyclins as well as direct inhibition of cyclin-CDK complexes by the CDK-inhibitor protein Sic1 (refs 1,2,3). Several striking similarities exist between Sic1 and Cdc6, a DNA replication factor essential for the formation of pre-replicative complexes at origins of DNA replication. Transcription of both genes is activated during late mitosis by a process dependent on Swi5 (ref. 10). Like Sic1, Cdc6 binds CDK complexes in vivo and downregulates them in vitro. Here we show that Cdc6, like Sic1, also contributes to inactivation of CDKs during late mitosis in S. cerevisiae. Deletion of the CDK-interacting domain of Cdc6 does not inhibit the function of origins of DNA replication during S phase, but instead causes a delay in mitotic exit; this delay is accentuated in the absence of Sic1 or of cyclin degradation. By contributing to mitotic exit and inactivation of CDKs, Cdc6 helps to create the conditions that are required for its subsequent role in the formation of pre-replicative complexes at origins of DNA replication.
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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.