ArticlePLoS genetics2009
Cdc7p-Dbf4p regulates mitotic exit by inhibiting Polo kinase.
Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 46 citations in OpenAlex.
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- Cdc5-mediated Ulp2 phosphorylation controls the timing of polySUMOylation during the cell cycle.The Journal of cell biology · 2026Article
- The prognostic significance and potential mechanism of DBF4 zinc finger in hepatocellular carcinoma.Scientific reports · 2024Article
- A function for ataxia telangiectasia and Rad3-related (ATR) kinase in cytokinetic abscission.iScience · 2022Article
- Structural Insight into the MCM double hexamer activation by Dbf4-Cdc7 kinase.Nature communications · 2022Article
- Identification and Validation of a Prognostic Model Based on Three MVI-Related Genes in Hepatocellular Carcinoma.International journal of biological sciences · 2022Article
- Cell-cycle phospho-regulation of the kinetochore.Current genetics · 2021Review
- Unifying the mechanism of mitotic exit control in a spatiotemporal logical model.PLoS biology · 2020Article
- Structural Basis for the Activation and Target Site Specificity of CDC7 Kinase.Structure (London, England : 1993) · 2020Article
- Pseudohyphal Growth of the Emerging Pathogen Candida auris Is Triggered by Genotoxic Stress through the S Phase Checkpoint.mSphere · 2020Article
- Distinct surfaces on Cdc5/PLK Polo-box domain orchestrate combinatorial substrate recognition during cell division.Scientific reports · 2020Article
- A Dual Inhibitor of Cdc7/Cdk9 Potently Suppresses T Cell Activation.Frontiers in immunology · 2019Article
- Functions and regulation of the Polo-like kinase Cdc5 in the absence and presence of DNA damage.Current genetics · 2018Review
- Fundamental cell cycle kinases collaborate to ensure timely destruction of the synaptonemal complex during meiosis.The EMBO journal · 2017Article
- DDK Promotes Tumor Chemoresistance and Survival via Multiple Pathways.Neoplasia (New York, N.Y.) · 2017Article
- Dbf4-dependent kinase and the Rtt107 scaffold promote Mus81-Mms4 resolvase activation during mitosis.The EMBO journal · 2017Article
- Understanding the Polo Kinase machine.Oncogene · 2015Review
- Pathway connectivity and signaling coordination in the yeast stress-activated signaling network.Molecular systems biology · 2014Article
- The budding yeast Polo-like kinase Cdc5 is released from the nucleus during anaphase for timely mitotic exit.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cdc7p-Dbf4p is a conserved protein kinase required for the initiation of DNA replication. The Dbf4p regulatory subunit binds Cdc7p and is essential for Cdc7p kinase activation, however, the N-terminal third of Dbf4p is dispensable for its essential replication activities. Here, we define a short N-terminal Dbf4p region that targets Cdc7p-Dbf4p kinase to Cdc5p, the single Polo kinase in budding yeast that regulates mitotic progression and cytokinesis. Dbf4p mediates an interaction with the Polo substrate-binding domain to inhibit its essential role during mitosis. Although Dbf4p does not inhibit Polo kinase activity, it nonetheless inhibits Polo-mediated activation of the mitotic exit network (MEN), presumably by altering Polo substrate targeting. In addition, although dbf4 mutants defective for interaction with Polo transit S-phase normally, they aberrantly segregate chromosomes following nuclear misorientation. Therefore, Cdc7p-Dbf4p prevents inappropriate exit from mitosis by inhibiting Polo kinase and functions in the spindle position checkpoint.
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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.