ReviewNature reviews. Molecular cell biology2013
Push back to respond better: regulatory inhibition of the DNA double-strand break response.
Review in Nature reviews. Molecular cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 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
104 citing papers in PubMed.
- Translating Host-Derived Signals from Cerebrospinal Fluid Metagenomic Sequencing into a Diagnostic Tool for Autoimmune Encephalitis in Children.Journal of clinical immunology · 2026Article
- The deubiquitinating enzyme Cezanne stabilizes BRCA1 by counteracting APC/C and Ube2S-dependent Lys11-linked ubiquitination.PLoS biology · 2025Article
- TRIP12's role in the governance of DNA polymerase β involvement in DNA damage response and repair.Nucleic acids research · 2025Article
- Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination.Biomolecules · 2025Article
- Host DNA damage and cellular fate in bacterial infections, with a focus on Staphylococcus aureus.FEMS microbiology reviews · 2025Review
- The Role of Ubiquitin-Proteasome System (UPS) in Asthma Pathology.Journal of asthma and allergy · 2025Review
- A benchmark of computational methods for correcting biases of established and unknown origin in CRISPR-Cas9 screening data.Genome biology · 2024Article
- The HDAC6-RNF168 axis regulates H2A/H2A.X ubiquitination to enable double-strand break repair.Nucleic acids research · 2023Article
- FBL promotes cancer cell resistance to DNA damage and BRCA1 transcription via YBX1.EMBO reports · 2023Article
- A sterol-PI(4)P exchanger modulates the Tel1/ATM axis of the DNA damage response.The EMBO journal · 2023Article
- DEtail-seq is an ultra-efficient and convenient method for meiotic DNA break profiling in multiple organisms.Science China. Life sciences · 2023Article
- An interactive web application for processing, correcting, and visualizing genome-wide pooled CRISPR-Cas9 screens.Cell reports methods · 2023Article
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
- Extracellular Release of Mitochondrial DNA: Triggered by Cigarette Smoke and Detected in COPD.Cells · 2022Article
- Co-opting regulation bypass repair as a gene-correction strategy for monogenic diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- RIF1 Links Replication Timing with Fork Reactivation and DNA Double-Strand Break Repair.International journal of molecular sciences · 2021Review
- VCP maintains nuclear size by regulating the DNA damage-associated MDC1-p53-autophagy axis in Drosophila.Nature communications · 2021Article
- ULK1 inhibition overcomes compromised antigen presentation and restores antitumor immunity in LKB1 mutant lung cancer.Nature cancer · 2021Article
- DNA repair pathways and their roles in drug resistance for lung adenocarcinoma.Molecular biology reports · 2021Review
- The complexity and regulation of repair of alkylation damage to nucleic acids.Critical reviews in biochemistry and molecular biology · 2021Review
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single DNA lesions such as DNA double-strand breaks (DSBs) can cause cell death or trigger genome rearrangements that have oncogenic potential, and so the pathways that mend and signal DNA damage must be highly sensitive but, at the same time, selective and reversible. When initiated, boundaries must be set to restrict the DSB response to the site of the lesion. The integration of positive and, crucially, negative control points involving post-translational modifications such as phosphorylation, ubiquitylation and acetylation is key for building fast, effective responses to DNA damage and for mitigating the impact of DNA lesions on genome integrity.
Indexed as
Identifiers
24002223What 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.