ArticleOncogene2002
Base excision repair of adenine/8-oxoguanine mispairs by an aphidicolin-sensitive DNA polymerase in human cell extracts.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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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
12 citing papers in PubMed, 24 citations in OpenAlex.
- The Response to Oxidative DNA Damage in Neurons: Mechanisms and Disease.Neural plasticity · 2016Review
- Functional activation of ATM by the prostate cancer suppressor NKX3.1.Cell reports · 2013Article
- Interaction of Sirt3 with OGG1 contributes to repair of mitochondrial DNA and protects from apoptotic cell death under oxidative stress.Cell death & disease · 2013Article
- MUTYH DNA glycosylase: the rationale for removing undamaged bases from the DNA.Frontiers in genetics · 2013Article
- Involvement of oxidatively damaged DNA and repair in cancer development and aging.American journal of translational research · 2010Article
- Single-nucleotide and long-patch base excision repair of DNA damage in plants.The Plant journal : for cell and molecular biology · 2009Article
- An 8-oxo-guanine repair pathway coordinated by MUTYH glycosylase and DNA polymerase lambda.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Replication protein A and proliferating cell nuclear antigen coordinate DNA polymerase selection in 8-oxo-guanine repair.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Article
- Futile short-patch DNA base excision repair of adenine:8-oxoguanine mispair.Nucleic acids research · 2004Article
- MUTYH prevents OGG1 or APEX1 from inappropriately processing its substrate or reaction product with its C-terminal domain.Nucleic acids research · 2004Article
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replication of DNA containing 8-oxo-7,8-dihydroguanine (8oxoG) can generate 8oxoG/A base pairs which, if uncorrected, lead to G-->T transversions. It is generally accepted that the repair of these promutagenic base pairs in human cells is initiated by the MutY DNA glycosylase homolog (hMYH). Here we provide biochemical evidence that human cell extracts perform base excision repair (BER) on both DNA strands of an 8oxoG/A mismatch. At early repair times the specificity of nucleotide incorporation indicates a preferential insertion of C opposite 8oxoG leading to the formation of 8oxoG/C pairs. This is followed by repair synthesis on the opposite DNA strand that is consistent with hOGG1-mediated correction of 8oxoG/C to G/C. Repair synthesis on either strand is completely inhibited by aphidicolin suggesting that a replicative DNA polymerase is involved in the gap filling. This is the first demonstration that repair of 8oxoG/A base pairs is by two BER events likely mediated by Poldelta/epsilon. We suggest that the Poldelta/epsilon-mediated BER is the general mode of repair when BER lesions are formed at replication forks.
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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.