ArticleNature2015
The core spliceosome as target and effector of non-canonical ATM signalling.
Article in Nature, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
168 citing papers in PubMed, 252 citations in OpenAlex.
- R-loops and D-loops: a delicate balance in genomic stability and instability.Cell communication and signaling : CCS · 2026Review
- Transcription-coupled nucleotide excision repair protects against genomic instability and cell death induced by the liver toxin methyleugenol.Cell death & disease · 2026Article
- Phosphorylation of SF3B1 by CDK11 orchestrates spliceosome activation via SNIP1-dependent RES complex recruitment.Nature communications · 2026Article
- ATM functions as a rheostat of metabolic stress in small-cell lung cancer.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- DGCR8 regulates multiple processes of transcription coupled nucleotide excision repair.Scientific reports · 2026Article
- Targeting MAT2A synergistically induces DNA damage in osteosarcoma cells through EZH2-mediated H3K27me3 modification.Journal of orthopaedic translation · 2025Article
- Crosstalk between chromatin state and ATM signalling in DNA damage-induced transcription stress.The EMBO journal · 2025Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Aquarius helicase facilitates HIV-1 integration into R-loop enriched genomic regions.Nature microbiology · 2025Article
- m6A modification in R-loop homeostasis: a potential target for cancer therapeutics.NAR cancer · 2025Review
- Review
- Article
- Metabolic Rewiring in the Face of Genomic Assault: Integrating DNA Damage Response and Cellular Metabolism.Biomolecules · 2025Review
- Cockayne syndrome B protein is implicated in transcription and associated chromatin dynamics in homeostatic and genotoxic conditions.Aging cell · 2025Article
- Looping forward: exploring R-loop processing and therapeutic potential.FEBS letters · 2025Review
- R-loops' m6A modification and its roles in cancers.Molecular cancer · 2024Review
- RNA biogenesis and RNA metabolism factors as R-loop suppressors: a hidden role in genome integrity.Genes & development · 2024Review
- Therapy-induced secretion of spliceosomal components mediates pro-survival crosstalk between ovarian cancer cells.Nature communications · 2024Article
- Transcription stress at telomeres leads to cytosolic DNA release and paracrine senescence.Nature communications · 2024Article
108 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
In response to DNA damage, tissue homoeostasis is ensured by protein networks promoting DNA repair, cell cycle arrest or apoptosis. DNA damage response signalling pathways coordinate these processes, partly by propagating gene-expression-modulating signals. DNA damage influences not only the abundance of messenger RNAs, but also their coding information through alternative splicing. Here we show that transcription-blocking DNA lesions promote chromatin displacement of late-stage spliceosomes and initiate a positive feedback loop centred on the signalling kinase ATM. We propose that initial spliceosome displacement and subsequent R-loop formation is triggered by pausing of RNA polymerase at DNA lesions. In turn, R-loops activate ATM, which signals to impede spliceosome organization further and augment ultraviolet-irradiation-triggered alternative splicing at the genome-wide level. Our findings define R-loop-dependent ATM activation by transcription-blocking lesions as an important event in the DNA damage response of non-replicating cells, and highlight a key role for spliceosome displacement in this process.
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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.