ReviewGenes2019
Control of Eukaryotic DNA Replication Initiation-Mechanisms to Ensure Smooth Transitions.
Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed.
- CDC7 and APC/CNature communications · 2026Article
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- A guide to the apicomplexan cell cycle: endodyogeny and schizogony.Trends in parasitology · 2025Review
- Loss of G1-phase CDK-inhibition biases instability between genomic regions by unevenly reducing activity among replication origins.iScience · 2025Article
- Regulation of replication timing in Saccharomyces cerevisiae.PLoS computational biology · 2025Article
- USP37 prevents unscheduled replisome unloading through MCM complex deubiquitination.Nature communications · 2025Article
- APC/C prevents a noncanonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Crk4-Cyc4 complex regulates GThe EMBO journal · 2024Article
- Unwinding Helicase MCM Functionality for Diagnosis and Therapeutics of Replication Abnormalities Associated with Cancer: A Review.Molecular diagnosis & therapy · 2024Review
- RAD51 restricts DNA over-replication from re-activated origins.The EMBO journal · 2024Article
- APC/C prevents non-canonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.bioRxiv : the preprint server for biology · 2023Article
- CDT1 inhibits CMG helicase in early S phase to separate origin licensing from DNA synthesis.Molecular cell · 2023Article
- Cell cycle exits and U-turns: Quiescence as multiple reversible forms of arrest.Faculty reviews · 2023Review
- Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions.Nature communications · 2022Article
- Review
- Two mechanisms of chromosome fragility at replication-termination sites in bacteria.Science advances · 2021Article
- Inhibition of DNA replication initiation by silver nanoclusters.Nucleic acids research · 2021Article
- Distinct and sequential re-replication barriers ensure precise genome duplication.PLoS genetics · 2020Article
- Mechanisms of eukaryotic replisome disassembly.Biochemical Society transactions · 2020Review
- Analysis of Differential Expression Proteins of Paclitaxel-Treated Lung Adenocarcinoma Cell A549 Using Tandem Mass Tag-Based Quantitative Proteomics.OncoTargets and therapy · 2020Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA replication differs from most other processes in biology in that any error will irreversibly change the nature of the cellular progeny. DNA replication initiation, therefore, is exquisitely controlled. Deregulation of this control can result in over-replication characterized by repeated initiation events at the same replication origin. Over-replication induces DNA damage and causes genomic instability. The principal mechanism counteracting over-replication in eukaryotes is a division of replication initiation into two steps-licensing and firing-which are temporally separated and occur at distinct cell cycle phases. Here, we review this temporal replication control with a specific focus on mechanisms ensuring the faultless transition between licensing and firing phases.
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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.