ArticleNucleic acids research2020
A distinct role for recombination repair factors in an early cellular response to transcription-replication conflicts.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed.
- TOPBP1-PLK1 interaction preserves genome integrity during mitosis.Nucleic acids research · 2026Article
- The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.Nucleic acids research · 2026Article
- Cyclin dependent kinase 9 inhibitor induces transcription-replication conflicts and DNA damage accumulation in breast cancer.Cancer cell international · 2025Article
- Transcription-replication conflicts drive R-loop-dependent nucleosome eviction and require DOT1L activity for transcription recovery.Nucleic acids research · 2025Article
- Synergistic effects of bloom helicase (BLM) inhibitor AO/854 with cisplatin in prostate cancer.Scientific reports · 2024Article
- The Fanconi anemia core complex promotes CtIP-dependent end resection to drive homologous recombination at DNA double-strand breaks.Nature communications · 2024Article
- OTUD5 limits replication fork instability by organizing chromatin remodelers.Nucleic acids research · 2023Article
- Fance deficiency inhibits primordial germ cell proliferation associated with transcription-replication conflicts accumulate and DNA repair defects.Journal of ovarian research · 2023Article
- FANCD2 promotes mitotic rescue from transcription-mediated replication stress in SETX-deficient cancer cells.Communications biology · 2022Article
- RAD18 opposes transcription-associated genome instability through FANCD2 recruitment.PLoS genetics · 2022Article
- Mitotic DNA synthesis is caused by transcription-replication conflicts in BRCA2-deficient cells.Molecular cell · 2022Article
- Genomic patterns of transcription-replication interactions in mouse primary B cells.Nucleic acids research · 2022Article
- A regulatory phosphorylation site on Mec1 controls chromatin occupancy of RNA polymerases during replication stress.The EMBO journal · 2021Article
- Transcription-Replication Collisions-A Series of Unfortunate Events.Biomolecules · 2021Review
- Intrinsic Disorder and Phosphorylation in BRCA2 Facilitate Tight Regulation of Multiple Conserved Binding Events.Biomolecules · 2021Review
- Consequences and Resolution of Transcription-Replication Conflicts.Life (Basel, Switzerland) · 2021Review
- Sites of chromosomal instability in the context of nuclear architecture and function.Cellular and molecular life sciences : CMLS · 2021Review
- Causes and consequences of RNA polymerase II stalling during transcript elongation.Nature reviews. Molecular cell biology · 2021Review
- RecQ helicases in DNA repair and cancer targets.Essays in biochemistry · 2020Review
- An emerging paradigm in epigenetic marking: coordination of transcription and replication.TranscriptionReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Transcription-replication (T-R) conflicts are profound threats to genome integrity. However, whilst much is known about the existence of T-R conflicts, our understanding of the genetic and temporal nature of how cells respond to them is poorly established. Here, we address this by characterizing the early cellular response to transient T-R conflicts (TRe). This response specifically requires the DNA recombination repair proteins BLM and BRCA2 as well as a non-canonical monoubiquitylation-independent function of FANCD2. A hallmark of the TRe response is the rapid co-localization of these three DNA repair factors at sites of T-R collisions. We find that the TRe response relies on basal activity of the ATR kinase, yet it does not lead to hyperactivation of this key checkpoint protein. Furthermore, specific abrogation of the TRe response leads to DNA damage in mitosis, and promotes chromosome instability and cell death. Collectively our findings identify a new role for these well-established tumor suppressor proteins at an early stage of the cellular response to conflicts between DNA transcription and replication.
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.