ArticleNature communications2018
Chromatin conformation regulates the coordination between DNA replication and transcription.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
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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
56 citing papers in PubMed, 102 citations in OpenAlex.
- ATP2B4 driven chromatin compaction exacerbates pancreatic cancer radiotherapy resistance.Cell death discovery · 2026Article
- H1.3 depletion in AML cells prompts H1.2 redistribution, chromatin remodeling and cell cycle defects.Epigenetics & chromatin · 2026Article
- Slow RNAPII elongation enhances naive pluripotency rewiring while maintaining high replication fork speed.Science advances · 2026Article
- Precise control of transcription condensates across S phase balances linker histone expression with DNA replication, ensuring genome stability.Molecular cell · 2026Article
- Design of bacterial DNT sensors based on computational models.Nucleic acids research · 2026Article
- Identification of small GTPases as potential target proteins of the mycotoxin and renal carcinogen ochratoxin A.Archives of toxicology · 2026Article
- Origin of chromosome 12 trisomy surge in human induced pluripotent stem cells.The Journal of cell biology · 2025Article
- Transcription-Replication Conflicts: Unlocking New Frontiers in Cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- EZH2-Mediated PHF10 Suppression Amplifies HMGB1/NF-κB Axis That Confers Chemotherapy Resistance in Cholangiocarcinoma.Journal of cellular and molecular medicine · 2025Article
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- Histone variant macroH2A1 regulates synchronous firing of replication origins in the inactive X chromosome.Nucleic acids research · 2024Article
- Genome-wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression.Genome biology · 2024Article
- Depletion of lamins B1 and B2 promotes chromatin mobility and induces differential gene expression by a mesoscale-motion-dependent mechanism.Genome biology · 2024Article
- Multiomics-integrated deep language model enables in silico genome-wide detection of transcription factor binding site in unexplored biosamples.Bioinformatics (Oxford, England) · 2024Article
- Review
- The research progress on radiation resistance of cervical cancer.Frontiers in oncology · 2024Review
- RNAPII-dependent ATM signaling at collisions with replication forks.Nature communications · 2023Article
- ORC1 binds to cis-transcribed RNAs for efficient activation of replication origins.Nature communications · 2023Article
- 3D chromatin connectivity underlies replication origin efficiency in mouse embryonic stem cells.Nucleic acids research · 2022Article
- Histone H1 regulates non-coding RNA turnover on chromatin in a m6A-dependent manner.Cell reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromatin is the template for the basic processes of replication and transcription, making the maintenance of chromosomal integrity critical for cell viability. To elucidate how dividing cells respond to alterations in chromatin structure, here we analyse the replication programme of primary cells with altered chromatin configuration caused by the genetic ablation of the HMGB1 gene, or three histone H1 genes. We find that loss of chromatin compaction in H1-depleted cells triggers the accumulation of stalled forks and DNA damage as a consequence of transcription-replication conflicts. In contrast, reductions in nucleosome occupancy due to the lack of HMGB1 cause faster fork progression without impacting the initiation landscape or fork stability. Thus, perturbations in chromatin integrity elicit a range of responses in the dynamics of DNA replication and transcription, with different consequences on replicative stress. These findings have broad implications for our understanding of how defects in chromatin structure contribute to genomic instability.
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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.