ReviewGenes2017
The Intra-S Checkpoint Responses to DNA Damage.
Review in Genes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 110 citations in OpenAlex.
- A CHK1-mediated phosphorylation switch suppresses human Topoisomerase 1-associated genomic instability.The EMBO journal · 2026Article
- Increased replication-associated single-stranded DNA promotes formaldehyde-induced mutagenesis.bioRxiv : the preprint server for biology · 2026Article
- DNAi: an open-source AI tool for unbiased DNA fiber analysis.Nucleic acids research · 2026Article
- Multiplexed TrAEL-seq captures DNA replication dynamics in mammalian cells.Nucleic acids research · 2026Article
- The RPA-binding domain and the KKRK motif in Rad26ATRIP cooperate at the perturbed DNA replication fork for initiating checkpoint signalling.PLoS genetics · 2026Article
- Cell Population Dynamics Informed by Cell-Cycle Regulation: A Deterministic Modeling Toolkit.Computational and structural biotechnology journal · 2026Review
- Interplay of replication timing, DNA repair, and translesion synthesis in UV mutagenesis in yeast.Nucleus (Austin, Tex.) · 2025Article
- The histone demethylase dLsd1 regulates organ size by silencing transposable elements.Communications biology · 2025Article
- Discovery of a DNA repair-associated radiosensitivity index for predicting radiotherapy efficacy in breast cancer.Frontiers in oncology · 2025Article
- Dissecting the Cell-Killing Mechanisms of Hydroxyurea Using Spot Assays.Methods in molecular biology (Clifton, N.J.) · 2025Article
- RAD18- and BRCA1-dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- Late fetal hematopoietic failure results from ZBTB11 deficiency despite abundant HSC specification.Blood advances · 2023Article
- Article
- DPPA5A suppresses the mutagenic TLS and MMEJ pathways by modulating the cryptic splicing ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Checkpoint Kinase 1 Is a Key Signal Transducer of DNA Damage in the Early Mammalian Cleavage Embryo.International journal of molecular sciences · 2023Review
- Article
- ASPM promotes ATR-CHK1 activation and stabilizes stalled replication forks in response to replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A genome-wide screen identifies SCAI as a modulator of the UV-induced replicative stress response.PLoS biology · 2022Article
- Rad53 arrests leading and lagging strand DNA synthesis via distinct mechanisms in response to DNA replication stress.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- Smc5/6 Complex Promotes Rad3Molecular and cellular biology · 2022Article
1 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Faithful duplication of the genome is a challenge because DNA is susceptible to damage by a number of intrinsic and extrinsic genotoxins, such as free radicals and UV light. Cells activate the intra-S checkpoint in response to damage during S phase to protect genomic integrity and ensure replication fidelity. The checkpoint prevents genomic instability mainly by regulating origin firing, fork progression, and transcription of G1/S genes in response to DNA damage. Several studies hint that regulation of forks is perhaps the most critical function of the intra-S checkpoint. However, the exact role of the checkpoint at replication forks has remained elusive and controversial. Is the checkpoint required for fork stability, or fork restart, or to prevent fork reversal or fork collapse, or activate repair at replication forks? What are the factors that the checkpoint targets at stalled replication forks? In this review, we will discuss the various pathways activated by the intra-S checkpoint in response to damage to prevent genomic instability.
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.