ArticleAging2010
A two-tiered compensatory response to loss of DNA repair modulates aging and stress response pathways.
Article in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Loss of DNA glycosylases improves health and cognitive function in a C. elegans model of human tauopathy.Nucleic acids research · 2024Article
- Review
- Base excision repair causes age-dependent accumulation of single-stranded DNA breaks that contribute to Parkinson disease pathology.Cell reports · 2021Article
- The Base Excision Repair Pathway in the NematodeFrontiers in cell and developmental biology · 2020Review
- Dysregulation of DAF-16/FOXO3A-mediated stress responses accelerates oxidative DNA damage induced aging.Redox biology · 2018Article
- Transcriptional consequences of XPA disruption in human cell lines.DNA repair · 2017Article
- Biomarkers of treatment toxicity in combined-modality cancer therapies with radiation and systemic drugs: study design, multiplex methods, molecular networks.International journal of molecular sciences · 2014Review
- Genome-wide analysis of gene expression in human embryonic tooth germ.Journal of molecular histology · 2014Article
- Article
- An increase of oxidised nucleotides activates DNA damage checkpoint pathway that regulates post-embryonic development in Caenorhabditis elegans.Mutagenesis · 2014Article
- DNA damage leads to progressive replicative decline but extends the life span of long-lived mutant animals.Cell death and differentiation · 2013Article
- Article
- Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1.Nucleic acids research · 2013Article
- Article
- Nucleoporin NUP153 guards genome integrity by promoting nuclear import of 53BP1.Cell death and differentiation · 2012Article
- Comparative interactomics with Funcoup 2.0.Nucleic acids research · 2012Article
- Untwisting of the DNA helix stimulates the endonuclease activity of Bacillus subtilis Nth at AP sites.Nucleic acids research · 2012Article
- Nucleotide Excision Repair in Caenorhabditis elegans.Molecular biology international · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we show that loss of NTH-1, the only Base Excision Repair (BER) enzyme known to initiate repair of oxidative DNA damage inC. elegans, restores normal lifespan of the short-lived NER deficient xpa-1 mutant. Loss of NTH-1 leads to oxidative stress and global expression profile changes that involve upregulation of genes responding to endogenous stress and downregulation of ILS. A similar, but more extensive, transcriptomic shift is observed in the xpa-1 mutant whereas loss of both NTH-1 and XPA-1 elicits a different profile with downregulation of Aurora-B and Polo-like kinase 1 signaling networks as well as DNA repair and DNA damage response genes. The restoration of normal lifespan and absence oxidative stress responses in nth-1;xpa-1 indicate that BER contributes to generate transcription blocking lesions from oxidative DNA damage. Hence, our data strongly suggests that the DNA lesions relevant for aging are repair intermediates resulting from aberrant or attempted processing by BER of lesions normally repaired by NER.
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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.