ArticleThe Journal of cell biology2010
Replication factory activation can be decoupled from the replication timing program by modulating Cdk levels.
Article in The Journal of cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 67 citations in OpenAlex.
- The role of DDK and Treslin-MTBP in coordinating replication licensing and pre-initiation complex formation.Open biology · 2021Article
- Organization of DNA Replication Origin Firing inGenes · 2021Article
- E2F-dependent transcription determines replication capacity and S phase length.Nature communications · 2020Article
- Chk1 loss creates replication barriers that compromise cell survival independently of excess origin firing.The EMBO journal · 2019Article
- Live imaging of marked chromosome regions reveals their dynamic resolution and compaction in mitosis.The Journal of cell biology · 2019Article
- Review
- The Protective Role of Dormant Origins in Response to Replicative Stress.International journal of molecular sciences · 2018Review
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- CDK activity provides temporal and quantitative cues for organizing genome duplication.PLoS genetics · 2018Article
- The essential kinase ATR: ensuring faithful duplication of a challenging genome.Nature reviews. Molecular cell biology · 2017Review
- Mutant p53 establishes targetable tumor dependency by promoting unscheduled replication.The Journal of clinical investigation · 2017Article
- Replicating Large Genomes: Divide and Conquer.Molecular cell · 2016Review
- Cyclin-dependent kinase regulates the length of S phase through TICRR/TRESLIN phosphorylation.Genes & development · 2015Article
- Chromatin structure and replication origins: determinants of chromosome replication and nuclear organization.Journal of molecular biology · 2014Review
- The contribution of dormant origins to genome stability: from cell biology to human genetics.DNA repair · 2014Review
- Uncovering the role of APC-Cdh1 in generating the dynamics of S-phase onset.Molecular biology of the cell · 2014Article
- Xenopus Cdc7 executes its essential function early in S phase and is counteracted by checkpoint-regulated protein phosphatase 1.Open biology · 2014Article
- From egg to gastrula: how the cell cycle is remodeled during the Drosophila mid-blastula transition.Annual review of genetics · 2014Review
- Dual phosphorylation of cdk1 coordinates cell proliferation with key developmental processes in Drosophila.Genetics · 2014Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
In the metazoan replication timing program, clusters of replication origins located in different subchromosomal domains fire at different times during S phase. We have used Xenopus laevis egg extracts to drive an accelerated replication timing program in mammalian nuclei. Although replicative stress caused checkpoint-induced slowing of the timing program, inhibition of checkpoint kinases in an unperturbed S phase did not accelerate it. Lowering cyclin-dependent kinase (Cdk) activity slowed both replication rate and progression through the timing program, whereas raising Cdk activity increased them. Surprisingly, modest alteration of Cdk activity changed the amount of DNA synthesized during different stages of the timing program. This was associated with a change in the number of active replication factories, whereas the distribution of origins within active factories remained relatively normal. The ability of Cdks to differentially effect replication initiation, factory activation, and progression through the timing program provides new insights into the way that chromosomal DNA replication is organized during S phase.
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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.