ReviewOncogene2002
Nijmegen breakage syndrome gene, NBS1, and molecular links to factors for genome stability.
Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 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
65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 207 citations in OpenAlex.
- Significant association between Nijmegen breakage syndrome 1 657del5 polymorphism and breast cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Pooled it
- Pooled it
- The BRCA1/2 pathway prevents hematologic cancers in addition to breast and ovarian cancers.BMC cancer · 2007Pooled it
- Spontaneous immortalization of bovine fibroblasts following long-term expansion offers a non-transformed cell source for cultivated beef.Nature food · 2025Article
- NBS1 facilitates preribosomal RNA biogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- DNA damage remodels the MITF interactome to increase melanoma genomic instability.Genes & development · 2024Article
- Interactions between the DNA Damage Response and the Telomere Complex in Carcinogenesis: A Hypothesis.Current issues in molecular biology · 2023Review
- A rad50 germline mutation induces tumorigenesis and ataxia-telangiectasia phenotype in a transparent medaka model.PloS one · 2023Article
- Critical DNA damaging pathways in tumorigenesis.Seminars in cancer biology · 2022Review
- NBS1-CtIP-mediated DNA end resection suppresses cGAS binding to micronuclei.Nucleic acids research · 2022Article
- Article
- RIF1 controls replication initiation and homologous recombination repair in a radiation dose-dependent manner.Journal of cell science · 2020Article
- Genome-wide association study identifies genetic susceptibility loci and pathways of radiation-induced acute oral mucositis.Journal of translational medicine · 2020Article
- PP4 deficiency leads to DNA replication stress that impairs immunoglobulin class switch efficiency.Cell death and differentiation · 2019Article
- Pellino1 regulates reversible ATM activation via NBS1 ubiquitination at DNA double-strand breaks.Nature communications · 2019Article
- Mechanistic link between DNA damage sensing, repairing and signaling factors and immune signaling.Advances in protein chemistry and structural biology · 2019Review
- Oxidative stress, mitochondrial abnormalities and antioxidant defense in Ataxia-telangiectasia, Bloom syndrome and Nijmegen breakage syndrome.Redox biology · 2017Review
- Sensitization strategies in lung cancer.Oncology letters · 2016Article
- NBS1 and multiple regulations of DNA damage response.Journal of radiation research · 2016Review
5 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
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks represent the most potentially serious damage to a genome and hence, at least two pathways of DNA repair have evolved; namely, homologous recombination repair and non-homologous end joining. Defects in both rejoining processes result in genomic instability including chromosome rearrangements, LOH and gene mutations, which may lead to development of malignancies. Nijmegen breakage syndrome is a recessive genetic disorder, characterized by elevated sensitivity to ionizing radiation that induces double-strand breaks, and high frequency of malignancies. NBS1, the product of the gene underlying the disease, forms a multimeric complex with hMRE11/hRAD50 nuclease and recruits them to the vicinity of sites of DNA damage by direct binding to phosphorylated histone H2AX. The combination of the highly-conserved NBS1 forkhead associated domain and BRCA1 C-terminus domain has a crucial role for recognition of damaged sites. Thereafter, the NBS1-complex proceeds to rejoin double-strand breaks predominantly by homologous recombination repair in vertebrates. This process collaborates with cell-cycle checkpoints at S and G2 phase to facilitate DNA repair. NBS1 is also associated with telomere maintenance and DNA replication. Based on recent knowledge regarding NBS1, we propose here a two-step binding mechanism for damage recognition by repair proteins, and describe the molecular links to factors for genome stability.
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.