ArticleCell cycle (Georgetown, Tex.)2010
DNA double-strand breaks and ATM activation by transcription-blocking DNA lesions.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 49 citations in OpenAlex.
- CF10 Displayed Improved Activity Relative to 5-FU in a Mouse CRLM Model Under Conditions of Physiological Folate.Cancers · 2025Article
- Article
- Human topoisomerases and their roles in genome stability and organization.Nature reviews. Molecular cell biology · 2022Review
- R-Loop-Associated Genomic Instability and Implication of WRN and WRNIP1.International journal of molecular sciences · 2022Review
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
- ATM pathway activation limits R-loop-associated genomic instability in Werner syndrome cells.Nucleic acids research · 2019Article
- The Cockayne syndrome protein B is involved in the repair of 5-AZA-2'-deoxycytidine-induced DNA lesions.Oncotarget · 2018Article
- PARP-1-dependent RND1 transcription induced by topoisomerase I cleavage complexes confers cellular resistance to camptothecin.Cell death & disease · 2018Article
- Structural basis for DNA 3'-end processing by human tyrosyl-DNA phosphodiesterase 1.Nature communications · 2018Article
- Plasticity of the Mre11-Rad50-Xrs2-Sae2 nuclease ensemble in the processing of DNA-bound obstacles.Genes & development · 2017Article
- Epigenetic changes in histone acetylation underpin resistance to the topoisomerase I inhibitor irinotecan.Nucleic acids research · 2017Article
- Neurological disorders associated with DNA strand-break processing enzymes.Mechanisms of ageing and development · 2017Review
- Roles of eukaryotic topoisomerases in transcription, replication and genomic stability.Nature reviews. Molecular cell biology · 2016Review
- DNA-PK triggers histone ubiquitination and signaling in response to DNA double-strand breaks produced during the repair of transcription-blocking topoisomerase I lesions.Nucleic acids research · 2016Article
- Chromatin remodeller SMARCA4 recruits topoisomerase 1 and suppresses transcription-associated genomic instability.Nature communications · 2016Article
- Dynamic Effects of Topoisomerase I Inhibition on R-Loops and Short Transcripts at Active Promoters.PloS one · 2016Article
- Flap Endonuclease 1 Limits Telomere Fragility on the Leading Strand.The Journal of biological chemistry · 2015Article
- Clinical and cellular roles for TDP1 and TOP1 in modulating colorectal cancer response to irinotecan.Molecular cancer therapeutics · 2015Article
- Repeat-mediated epigenetic dysregulation of the FMR1 gene in the fragile X-related disorders.Frontiers in genetics · 2015Review
- TDP1/TOP1 Ratio as a Promising Indicator for the Response of Small Cell Lung Cancer to Topotecan.Journal of cancer science & therapy · 2014Article
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 at 2 institutions in 2 countries.
Funding
Abstract
A taxia telangiectasia mutated (ATM), the deficiency of which causes a severe neurodegenerative disease, is a crucial mediator for the DNA double-strand break (DSB) response. We recently showed that transcription-blocking topoisomerase I cleavage complexes (TOP1cc) produce DSBs related to R-loop formation and activate ATM in post-mitotic neurons and lymphocytes. Here we discuss how TOP1cc can produce transcription arrest with R-loop formation and generate DSBs that activate ATM, as well as data suggesting that those transcription-dependent DSBs tend to form at the IgH locus and at specific genomic sites. We also address the potential roles of ATM in response to transcription-blocking TOP1cc.
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.