ReviewThe EMBO journal2010
Mechanisms and regulation of DNA end resection.
Review in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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
62 citing papers in PubMed, 1 synthesis or guideline pooled it.
- LncRNAs-associated to genomic instability: A barrier to cancer therapy effectiveness.Frontiers in genetics · 2022Pooled it
- Biochemical Mechanisms of Genetic Recombination and DNA Repair.Annual review of biochemistry · 2025Review
- Helicase HELQ: Molecular Characters Fit for DSB Repair Function.International journal of molecular sciences · 2024Review
- The cGAS-Ku80 complex regulates the balance between two end joining subpathways.Cell death and differentiation · 2024Article
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- The telomerase inhibitor imetelstat differentially targets JAK2V617F versus CALR mutant myeloproliferative neoplasm cells and inhibits JAK-STAT signaling.Frontiers in oncology · 2023Article
- SIAH2 regulates DNA end resection and replication fork recovery by promoting CtIP ubiquitination.Nucleic acids research · 2022Article
- The Finely Coordinated Action of SSB and NurA/HerA Complex Strictly Regulates the DNA End Resection Process inInternational journal of molecular sciences · 2022Article
- Genetic Variants in Double-Strand Break Repair Pathway Genes to Predict Platinum-Based Chemotherapy Prognosis in Patients With Lung Cancer.Frontiers in pharmacology · 2022Article
- Article
- A stapled peptide mimetic of the CtIP tetramerization motif interferes with double-strand break repair and replication fork protection.Science advances · 2021Article
- Review
- Recombinational Repair of Nuclease-Generated Mitotic Double-Strand Breaks with Different End Structures in Yeast.G3 (Bethesda, Md.) · 2020Article
- DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells.Experimental & molecular medicine · 2020Review
- Cell Cycle and DNA Repair Regulation in the Damage Response: Protein Phosphatases Take Over the Reins.International journal of molecular sciences · 2020Review
- Inhibition of FGFR2-Signaling Attenuates a Homology-Mediated DNA Repair in GIST and Sensitizes Them to DNA-Topoisomerase II Inhibitors.International journal of molecular sciences · 2020Article
- Article
- CtIP is essential for telomere replication.Nucleic acids research · 2019Article
- Pellino1 regulates reversible ATM activation via NBS1 ubiquitination at DNA double-strand breaks.Nature communications · 2019Article
- PARPi Triggers the STING-Dependent Immune Response and Enhances the Therapeutic Efficacy of Immune Checkpoint Blockade Independent of BRCAness.Cancer research · 2019Article
2 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) are highly hazardous for genome integrity, because failure to repair these lesions can lead to genomic instability. DSBs can arise accidentally at unpredictable locations into the genome, but they are also normal intermediates in meiotic recombination. Moreover, the natural ends of linear chromosomes resemble DSBs. Although intrachromosomal DNA breaks are potent stimulators of the DNA damage response, the natural ends of linear chromosomes are packaged into protective structures called telomeres that suppress DNA repair/recombination activities. Although DSBs and telomeres are functionally different, they both undergo 5'-3' nucleolytic degradation of DNA ends, a process known as resection. The resulting 3'-single-stranded DNA overhangs enable repair of DSBs by homologous recombination (HR), whereas they allow the action of telomerase at telomeres. The molecular activities required for DSB and telomere end resection are similar, indicating that the initial steps of HR and telomerase-mediated elongation are related. Resection of both DSBs and telomeres must be tightly regulated in time and space to ensure genome stability and cell survival.
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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.