ArticleNucleic acids research2015
Complementation of aprataxin deficiency by base excision repair enzymes.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Repair pathway coordination from gap filling by polβ and subsequent nick sealing by LIG1 or LIG3α governs BER efficiency at the downstream steps.DNA repair · 2025Article
- Impact of DNA ligase inhibition on the nick sealing of polβ nucleotide insertion products at the downstream steps of base excision repair pathway.Mutagenesis · 2024Article
- Structures of LIG1 that engage with mutagenic mismatches inserted by polβ in base excision repair.Nature communications · 2022Article
- DNA ligase I variants fail in the ligation of mutagenic repair intermediates with mismatches and oxidative DNA damage.Mutagenesis · 2020Article
- Pol β gap filling, DNA ligation and substrate-product channeling during base excision repair opposite oxidized 5-methylcytosine modifications.DNA repair · 2020Article
- The ligation of pol β mismatch insertion products governs the formation of promutagenic base excision DNA repair intermediates.Nucleic acids research · 2020Article
- Interplay between DNA Polymerases and DNA Ligases: Influence on Substrate Channeling and the Fidelity of DNA Ligation.Journal of molecular biology · 2019Review
- Deoxyribonucleic Acid Damage and Repair: Capitalizing on Our Understanding of the Mechanisms of Maintaining Genomic Integrity for Therapeutic Purposes.International journal of molecular sciences · 2018Review
- XRCC1 phosphorylation affects aprataxin recruitment and DNA deadenylation activity.DNA repair · 2018Article
- Complementation of aprataxin deficiency by base excision repair enzymes in mitochondrial extracts.Nucleic acids research · 2017Article
- Article
- Oxidized nucleotide insertion by pol β confounds ligation during base excision repair.Nature communications · 2017Article
- Chronic oxidative damage together with genome repair deficiency in the neurons is a double whammy for neurodegeneration: Is damage response signaling a potential therapeutic target?Mechanisms of ageing and development · 2017Review
- Neurological disorders associated with DNA strand-break processing enzymes.Mechanisms of ageing and development · 2017Review
- Linking DNA polymerase theta structure and function in health and disease.Cellular and molecular life sciences : CMLS · 2016Article
- Reprint of "Oxidant and environmental toxicant-induced effects compromise DNA ligation during base excision DNA repair".DNA repair · 2015Review
- Oxidant and environmental toxicant-induced effects compromise DNA ligation during base excision DNA repair.DNA repair · 2015Review
- DNA ligase I fidelity mediates the mutagenic ligation of pol β oxidized and mismatch nucleotide insertion products in base excision repair.The Journal of biological chemistryArticle
- Enzymatic Activity Assays for Base Excision Repair Enzymes in Cell Extracts from Vertebrate Cells.Bio-protocolArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Abortive ligation during base excision repair (BER) leads to blocked repair intermediates containing a 5'-adenylated-deoxyribose phosphate (5'-AMP-dRP) group. Aprataxin (APTX) is able to remove the AMP group allowing repair to proceed. Earlier results had indicated that purified DNA polymerase β (pol β) removes the entire 5'-AMP-dRP group through its lyase activity and flap endonuclease 1 (FEN1) excises the 5'-AMP-dRP group along with one or two nucleotides. Here, using cell extracts from APTX-deficient cell lines, human Ataxia with Oculomotor Apraxia Type 1 (AOA1) and DT40 chicken B cell, we found that pol β and FEN1 enzymatic activities were prominent and strong enough to complement APTX deficiency. In addition, pol β, APTX and FEN1 coordinate with each other in processing of the 5'-adenylated dRP-containing BER intermediate. Finally, other DNA polymerases and a repair factor with dRP lyase activity (pol λ, pol ι, pol θ and Ku70) were found to remove the 5'-adenylated-dRP group from the BER intermediate. However, the activities of these enzymes were weak compared with those of pol β and FEN1.
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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.