ReviewNature chemical biology2025
Decoding replication stress responses through post-translational modifications.
Review in Nature chemical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- A BIN2-SOG1 molecular module regulates replication stress response independently on ATR.Science advances · 2026Article
- Mutant p53 Directs PARP to Regulate Replication Stress and Drive Breast Cancer Metastasis.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
DNA replication is a fundamental cellular process that ensures the faithful duplication of the genome during cell division. However, this process is frequently challenged by various intrinsic and extrinsic factors that can impede replication fork progression and jeopardize genomic integrity. To safeguard against these challenges, cells have evolved intricate stress response mechanisms, including replication checkpoint activation, translesion DNA synthesis, repriming and fork reversal, all of which are vital for preserving genomic stability. Central to the orchestration of these pathways are post-translational modifications (PTMs), which dynamically regulate the stability, localization, and activity of key proteins involved in the replication stress responses. In this Review, we summarize the primary mechanisms that orchestrate cellular responses to replication stress and highlight emerging insights into the roles of both histone and nonhistone PTMs in the precise and coordinated regulation of replication fork dynamics under genotoxic conditions.
Indexed as
Identifiers
41057601What 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.