ReviewCarcinogenesis2014
Base excision repair capacity in informing healthspan.
Review in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 46 citations in OpenAlex.
- Hypomorphic Protein Expression of DNA Polymerase Beta in PolβBiomolecules · 2026Article
- DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023Review
- AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations.Environmental and molecular mutagenesis · 2022Article
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Versatile cell-based assay for measuring DNA alkylation damage and its repair.Scientific reports · 2021Article
- Molecular Mechanisms Regulating the DNA Repair Protein APE1: A Focus on Its Flexible N-Terminal Tail Domain.International journal of molecular sciences · 2021Review
- Focus on DNA Glycosylases-A Set of Tightly Regulated Enzymes with a High Potential as Anticancer Drug Targets.International journal of molecular sciences · 2020Review
- Non-muscle invasive bladder cancer tissues have increased base excision repair capacity.Scientific reports · 2020Article
- A Multi-Endpoint Approach to Base Excision Repair Incision Activity Augmented by PARylation and DNA Damage Levels in Mice: Impact of Sex and Age.International journal of molecular sciences · 2020Article
- Functions of the major abasic endonuclease (APE1) in cell viability and genotoxin resistance.Mutagenesis · 2020Review
- DNA Damage and Associated DNA Repair Defects in Disease and Premature Aging.American journal of human genetics · 2019Review
- DNA Repair Molecular Beacon assay: a platform for real-time functional analysis of cellular DNA repair capacity.Oncotarget · 2018Article
- APE1 deficiency promotes cellular senescence and premature aging features.Nucleic acids research · 2018Article
- OGG1-initiated base excision repair exacerbates oxidative stress-induced parthanatos.Cell death & disease · 2018Article
- Heat shock proteins and DNA repair mechanisms: an updated overview.Cell stress & chaperones · 2018Review
- Review
- In vivo measurements of interindividual differences in DNA glycosylases and APE1 activities.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Development of a Cell-Based Assay for Measuring Base Excision Repair Responses.Scientific reports · 2017Article
- Imaging the DNA damage response with PET and SPECT.European journal of nuclear medicine and molecular imaging · 2017Review
- Coordination of DNA single strand break repair.Free radical biology & medicine · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Base excision repair (BER) is a frontline defense mechanism for dealing with many common forms of endogenous DNA damage, several of which can drive mutagenic or cell death outcomes. The pathway engages proteins such as glycosylases, abasic endonucleases, polymerases and ligases to remove substrate modifications from DNA and restore the genome back to its original state. Inherited mutations in genes related to BER can give rise to disorders involving cancer, immunodeficiency and neurodegeneration. Studies employing genetically defined heterozygous (haploinsufficient) mouse models indicate that partial reduction in BER capacity can increase vulnerability to both spontaneous and exposure-dependent pathologies. In humans, measurement of BER variation has been imperfect to this point, yet tools to assess BER in epidemiological surveys are steadily evolving. We provide herein an overview of the BER pathway and discuss the current efforts toward defining the relationship of BER defects with disease susceptibility.
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.