ReviewJournal of cellular biochemistry2006
The cellular control of DNA double-strand breaks.
Review in Journal of cellular biochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 53 papers, 2 of them syntheses 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
53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.
- The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025Pooled it
- NBS1 Glu185Gln polymorphism and cancer risk: update on current evidence.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Loss of DNA-PK complex in recurrent pterygium suggests a role for defective double-strand break repair.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026Article
- SFPQ Promotes Homologous Recombination via mRNA Stabilization of RAD51 and Its Paralogs.Journal of molecular biology · 2026Article
- SFPQ Promotes Homologous Recombination via mRNA Stabilization of RAD51 and Its Paralogs.bioRxiv : the preprint server for biology · 2025Article
- Contribution of MRE11, RAD50, and NBS1 Genotypes to Bladder Cancer Susceptibility.Cancer genomics & proteomics · 2025Article
- Mechanisms of the FLASH effect: current insights and advances.Frontiers in cell and developmental biology · 2025Review
- Bridging the gap: R-loop mediated genomic instability and its implications in neurological diseases.Epigenomics · 2024Review
- Developmental progression of DNA double-strand break repair deciphered by a single-allele resolution mutation classifier.Nature communications · 2024Article
- Chloroquine-induced DNA damage synergizes with DNA repair inhibitors causing cancer cell death.Frontiers in oncology · 2024Article
- Mitochondrial Signaling Pathways Associated with DNA Damage Responses.International journal of molecular sciences · 2023Review
- DNA damage response signaling: A common link between cancer and cardiovascular diseases.Cancer medicine · 2023Review
- Comprehensive comparison between azacytidine and decitabine treatment in an acute myeloid leukemia cell line.Clinical epigenetics · 2022Article
- Chloroquine-Induced DNA Damage Synergizes with Nonhomologous End Joining Inhibition to Cause Ovarian Cancer Cell Cytotoxicity.International journal of molecular sciences · 2022Article
- Epigenetic Anti-Cancer Treatment With a Stabilized Carbocyclic Decitabine Analogue.Chemistry (Weinheim an der Bergstrasse, Germany) · 2022Article
- Review
- Review
- Autism-Associated Vigilin Depletion Impairs DNA Damage Repair.Molecular and cellular biology · 2021Article
- Synergistic effect of Chloroquine and Panobinostat in ovarian cancer through induction of DNA damage and inhibition of DNA repair.Neoplasia (New York, N.Y.) · 2021Article
- spn-A/rad51 mutant exhibits enhanced genomic damage, cell death and low temperature sensitivity in somatic tissues.Chromosoma · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA double-strand breaks (DSBs) are the most hazardous lesions arising in the genome of eukaryotic organisms, and yet occur normally during DNA replication, meiosis, and immune system development. The efficient repair of DSBs is crucial in maintaining genomic integrity, cellular viability, and the prevention of tumorigenesis. As a consequence, eukaryotic cells have evolved efficient mechanisms that sense and respond to DSBs and ultimately repair the break. The swiftness of the DNA DSB response has paved to the identification of sensors and transducers which allowed to generate a hierarchical signaling paradigm depicting the transduction of the damage signal to numerous downstream effectors (Fig. 1). The function of such effectors involve posttranslational modifications through phosphorylation, acetylation, and methylation of the substrates. This review will address the control of DSBs in damaged eukaryotic cells, the physiological processes that require the introduction of a DSB into the genome, and the maintenance of DSBs in non-damaged cells.
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.