ReviewDNA repair2008
Nucleotide excision repair deficient mouse models 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 21 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
21 citing papers in PubMed, 46 citations in OpenAlex.
- Unraveling the intersection of aging and Parkinson's disease: a collaborative roadmap for advancing research models.NPJ Parkinson's disease · 2026Review
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Persistent TFIIH binding to non-excised DNA damage causes cell and developmental failure.Nature communications · 2024Article
- DNA damage and regulation of protein homeostasis.DNA repair · 2021Review
- Activation of the DNA damage response in vivo in synucleinopathy models of Parkinson's disease.Cell death & disease · 2018Article
- Identification of HSP90 inhibitors as a novel class of senolytics.Nature communications · 2017Article
- ERCC1-XPF cooperates with CTCF and cohesin to facilitate the developmental silencing of imprinted genes.Nature cell biology · 2017Article
- Inefficient DNA Repair Is an Aging-Related Modifier of Parkinson's Disease.Cell reports · 2016Article
- Mutations in Cockayne Syndrome-Associated Genes (Csa and Csb) Predispose to Cisplatin-Induced Hearing Loss in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Inhibitors of histone deacetylases enhance neurotoxicity of DNA damage.Neuromolecular medicine · 2014Article
- Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency.PLoS genetics · 2014Article
- Understanding nucleotide excision repair and its roles in cancer and ageing.Nature reviews. Molecular cell biology · 2014Review
- Atrx deficiency induces telomere dysfunction, endocrine defects, and reduced life span.The Journal of clinical investigation · 2013Article
- Downregulation of cholesterol biosynthesis genes in the forebrain of ERCC1-deficient mice.Neurobiology of disease · 2012Article
- Defective transcription initiation causes postnatal growth failure in a mouse model of nucleotide excision repair (NER) progeria.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Age-related neuronal degeneration: complementary roles of nucleotide excision repair and transcription-coupled repair in preventing neuropathology.PLoS genetics · 2011Article
- Ocular manifestations of trichothiodystrophy.Ophthalmology · 2011Article
- Premature aging-related peripheral neuropathy in a mouse model of progeria.Mechanisms of ageing and development · 2011Article
- Nucleotide Excision Repair in Caenorhabditis elegans.Molecular biology international · 2011Article
- Age-related motor neuron degeneration in DNA repair-deficient Ercc1 mice.Acta neuropathologica · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Nucleotide excision repair (NER) is a highly conserved mechanism to remove helix-distorting DNA base damage. A major substrate for NER is DNA damage caused by environmental genotoxins, most notably ultraviolet radiation. Xeroderma pigmentosum, Cockayne syndrome and trichothiodystrophy are three human diseases caused by inherited defects in NER. The symptoms and severity of these diseases vary dramatically, ranging from profound developmental delay to cancer predisposition and accelerated aging. All three syndromes include neurological disease, indicating an important role for NER in protecting against spontaneous DNA damage as well. To study the pathophysiology caused by DNA damage, numerous mouse models of NER-deficiency were generated by knocking-out genes required for NER or knocking-in disease-causing human mutations. This review explores the utility of these mouse models to study neurological disease caused by NER-deficiency.
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.