ArticleNucleic acids research2011
A novel regulatory circuit in base excision repair involving AP endonuclease 1, Creb1 and DNA polymerase beta.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 28 citations in OpenAlex.
- Frying oils with high natural or added antioxidants content, which protect against postprandial oxidative stress, also protect against DNA oxidation damage.European journal of nutrition · 2017Trial
- Zebrafish Polymerase Theta and human Polymerase Theta: Orthologues with homologous function.PloS one · 2025Article
- DNA repair genes play a variety of roles in the development of fish embryos.Frontiers in cell and developmental biology · 2023Review
- RETRACTED: Combined Effects of Potassium Perchlorate and a Neonicotinoid on Zebrafish Larvae (Toxics · 2022Article
- Species variations in XRCC1 recruitment strategies for FHA domain-containing proteins.DNA repair · 2022Article
- Article
- AP endonuclease 1 (Apex1) influences brain development linking oxidative stress and DNA repair.Cell death & disease · 2019Article
- Transcription Factors and DNA Repair Enzymes Compete for Damaged Promoter Sites.The Journal of biological chemistry · 2016Article
- TCRP1 contributes to cisplatin resistance by preventing Pol β degradation in lung cancer cells.Molecular and cellular biochemistry · 2015Article
- Identification and characterization of human apurinic/apyrimidinic endonuclease-1 inhibitors.Biochemistry · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
DNA repair is required to maintain genome stability in stem cells and early embryos. At critical junctures, oxidative damage to DNA requires the base excision repair (BER) pathway. Since early zebrafish embryos lack the major polymerase in BER, DNA polymerase ß, repair proceeds via replicative polymerases, even though there is ample polb mRNA. Here, we report that Polb protein fails to appear at the appropriate time in development when AP endonuclease 1 (Apex), the upstream protein in BER, is knocked down. Because polb contains a Creb1 binding site, we examined whether knockdown of Apex affects creb1. Apex knockdown results in loss of Creb1 and Creb complex members but not Creb1 phosphorylation. This effect is independent of p53. Although both apex and creb1 mRNA rescue Creb1 and Polb after Apex knockdown, Apex is not a co-activator of creb1 transcription. This observation has broad significance, as similar results occur when Apex is inhibited in B cells from apex(+/-) mice. These results describe a novel regulatory circuit involving Apex, Creb1 and Polb and provide a mechanism for lethality of Apex loss in higher eukaryotes.
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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.