ArticleMolecular cell2010
Mec1 is one of multiple kinases that prime the Mcm2-7 helicase for phosphorylation by Cdc7.
Article in Molecular cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
117 citing papers in PubMed, 165 citations in OpenAlex.
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- CDC7 is a targetable regulator of advanced prostate cancer.Scientific reports · 2025Article
- Phosphatase specificity influences phosphorylation timing of CDK substrates during the cell cycle.Nature communications · 2025Article
- Clinical significance and pro-oncogenic function of DBF4 in clear cell renal cell carcinoma.BMC urology · 2025Article
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- Novel role of DONSON in CMG helicase assembly during vertebrate DNA replication initiation.The EMBO journal · 2023Article
- Article
- Review
- The Role of MTBP as a Replication Origin Firing Factor.Biology · 2022Review
- The structural basis of Cdc7-Dbf4 kinase dependent targeting and phosphorylation of the MCM2-7 double hexamer.Nature communications · 2022Article
- Structural Insight into the MCM double hexamer activation by Dbf4-Cdc7 kinase.Nature communications · 2022Article
- Multiple roles of Pol epsilon in eukaryotic chromosome replication.Biochemical Society transactions · 2022Article
- Structural mechanism for the selective phosphorylation of DNA-loaded MCM double hexamers by the Dbf4-dependent kinase.Nature structural & molecular biology · 2022Article
- Cdc7-mediated phosphorylation of Cse4 regulates high-fidelity chromosome segregation in budding yeast.Molecular biology of the cell · 2021Article
- A basal-level activity of ATR links replication fork surveillance and stress response.Molecular cell · 2021Article
- Novel insights into the mechanism of cell cycle kinases Mec1(ATR) and Tel1(ATM).Critical reviews in biochemistry and molecular biology · 2021Article
- Replication initiation: Implications in genome integrity.DNA repair · 2021Review
- Meikin synergizes with shugoshin to protect cohesin Rec8 during meiosis I.Genes & development · 2021Article
- DDK regulates replication initiation by controlling the multiplicity of Cdc45-GINS binding to Mcm2-7.eLife · 2021Article
- MTBP phosphorylation controls DNA replication origin firing.Scientific reports · 2021Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of the eukaryotic replicative DNA helicase, the Mcm2-7 complex, requires phosphorylation by Cdc7/Dbf4 (Dbf4-dependent kinase or DDK), which, in turn, depends on prior phosphorylation of Mcm2-7 by an unknown kinase (or kinases). We identified DDK phosphorylation sites on Mcm4 and Mcm6 and found that phosphorylation of either subunit suffices for cell proliferation. Importantly, prior phosphorylation of either S/T-P or S/T-Q motifs on these subunits is required for DDK phosphorylation of Mcm2-7 and for normal S phase passage. Phosphomimetic mutations of DDK target sites bypass both DDK function and mutation of the priming phosphorylation sites. Mrc1 facilitates Mec1 phosphorylation of the S/T-Q motifs of chromatin-bound Mcm2-7 during S phase to activate replication. Genetic interactions between priming site mutations and MRC1 or TOF1 deletion support a role for these modifications in replication fork stability. These findings identify regulatory mechanisms that modulate origin firing and replication fork assembly during cell cycle progression.
Indexed as
Identifiers
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.