ArticleeLife2020
Antagonistic control of DDK binding to licensed replication origins by Mcm2 and Rad53.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- Dbf4-dependent kinase finetunes Ino80 function at chromosome replication origins.Nature communications · 2026Article
- Selective interactions at pre-replication complexes categorize baseline and dormant origins.Nature communications · 2025Article
- G-quadruplex-stalled eukaryotic replisome structure reveals helical inchworm DNA translocation.Science (New York, N.Y.) · 2025Article
- Review
- DDK: The Outsourced Kinase of Chromosome Maintenance.Biology · 2022Review
- The structural basis of Cdc7-Dbf4 kinase dependent targeting and phosphorylation of the MCM2-7 double hexamer.Nature communications · 2022Article
- Structural mechanism for the selective phosphorylation of DNA-loaded MCM double hexamers by the Dbf4-dependent kinase.Nature structural & molecular biology · 2022Article
- Dbf4-Dependent Kinase: DDK-ated to post-initiation events in DNA replication.Cell cycle (Georgetown, Tex.) · 2021Review
- Rad53 checkpoint kinase regulation of DNA replication fork rate via Mrc1 phosphorylation.eLife · 2021Article
- DDK regulates replication initiation by controlling the multiplicity of Cdc45-GINS binding to Mcm2-7.eLife · 2021Article
- Checkpoint inhibition of origin firing prevents inappropriate replication outside of S-phase.eLife · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Eukaryotic replication origins are licensed by the loading of the replicative DNA helicase, Mcm2-7, in inactive double hexameric form around DNA. Subsequent origin activation is under control of multiple protein kinases that either promote or inhibit origin activation, which is important for genome maintenance. Using the reconstituted budding yeast DNA replication system, we find that the flexible N-terminal extension (NTE) of Mcm2 promotes the stable recruitment of Dbf4-dependent kinase (DDK) to Mcm2-7 double hexamers, which in turn promotes DDK phosphorylation of Mcm4 and -6 and subsequent origin activation. Conversely, we demonstrate that the checkpoint kinase, Rad53, inhibits DDK binding to Mcm2-7 double hexamers. Unexpectedly, this function is not dependent on Rad53 kinase activity, suggesting steric inhibition of DDK by activated Rad53. These findings identify critical determinants of the origin activation reaction and uncover a novel mechanism for checkpoint-dependent origin inhibition.
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What OpenQuestion holds
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.