ReviewDNA repair2008
Mouse models of DNA double-strand break repair and neurological disease.
Review in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 48 citations in OpenAlex.
- Nickase NmCas9 unsilences paternal Ube3a in a mouse model of Angelman syndrome without causing AAV vector integration.Scientific reports · 2026Article
- Base excision repair and double strand break repair cooperate to modulate the formation of unrepaired double strand breaks in mouse brain.Nature communications · 2024Article
- Review
- Automated Immunofluorescence Staining for Analysis of DNA Damage and Apoptosis in Brain Sections.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Processing Neonatal Mouse Brains for Immunohistochemical Analysis: As Required for Including Spindle Orientation Analysis and Analysis of DNA Damage and Apoptosis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- LINE-1 and Alu methylation signatures in autism spectrum disorder and their associations with the expression of autism-related genes.Scientific reports · 2022Article
- Exploring the Origin and Physiological Significance of DNA Double Strand Breaks in the Developing Neuroretina.International journal of molecular sciences · 2022Review
- Species variations in XRCC1 recruitment strategies for FHA domain-containing proteins.DNA repair · 2022Article
- An Eye in the Replication Stress Response: Lessons From Tissue-Specific StudiesFrontiers in cell and developmental biology · 2021Review
- ATRIP protects progenitor cells against DNA damage in vivo.Cell death & disease · 2020Article
- Review
- Suppressor mutations inGenome research · 2020Article
- Loss of H3K36 Methyltransferase SETD2 Impairs V(D)J Recombination during Lymphoid Development.iScience · 2020Article
- RINT1 Loss Impairs Retinogenesis Through TRP53-Mediated Apoptosis.Frontiers in cell and developmental biology · 2020Article
- DNA methylation patterns of LINE-1 and Alu for pre-symptomatic dementia in type 2 diabetes.PloS one · 2020Article
- RAG-2 deficiency results in fewer phosphorylated histone H2AX foci, but increased retinal ganglion cell death and altered axonal growth.Scientific reports · 2019Article
- Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases.Current neuropharmacology · 2019Review
- Expression Levels of Two DNA Repair-related Genes under 8 Gy Ionizing Radiation and 100 Mg/Kg Melatonin Delivery In Rat Peripheral Blood.Journal of biomedical physics & engineering · 2017Article
- Increased neuronal death and disturbed axonal growth in the Polμ-deficient mouse embryonic retina.Scientific reports · 2016Article
- Epidermal Nbn deletion causes premature hair loss and a phenotype resembling psoriasiform dermatitis.Oncotarget · 2016Article
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 at 1 institution in 1 country.
Funding
Abstract
The repair of DNA damage is essential for the prevention of disease. The DNA double-strand break (DSB) is a particularly hazardous lesion. DNA DSBs activate a coordinated cellular response involving cell cycle checkpoint activation and repair of the DNA break, or alternatively apoptosis. In the nervous system the inability to respond to DNA DSBs may lead to neurodegenerative disease or brain tumors. Therefore, understanding the DNA DSB response mechanism in the nervous system is of high importance for developing new treatments for neurodegeneration and cancer. In this regard, the use of mouse models represents an important approach for advancing our understanding of the biology of the DNA damage response in the nervous system.
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.