ArticleDNA repair2010
Genetic interactions between HNT3/Aprataxin and RAD27/FEN1 suggest parallel pathways for 5' end processing during base excision repair.
Article in DNA repair, 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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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Stable Hypermutators Revealed by the Genomic Landscape of Genes Involved in Genome Stability Among Yeast Species.Molecular biology and evolution · 2025Article
- Induced pluripotent stem cells carrying novel APTX mutations presented defective neural differentiation with the accumulation of DNA single-strand breaks.Cell death discovery · 2025Article
- TORC2 inhibition triggers yeast chromosome fragmentation through misregulated Base Excision Repair of clustered oxidation events.Nature communications · 2024Article
- The base excision repair process: comparison between higher and lower eukaryotes.Cellular and molecular life sciences : CMLS · 2021Review
- Mechanism of APTX nicked DNA sensing and pleiotropic inactivation in neurodegenerative disease.The EMBO journal · 2018Article
- Neurological disorders associated with DNA strand-break processing enzymes.Mechanisms of ageing and development · 2017Review
- Slow mitochondrial repair of 5'-AMP renders mtDNA susceptible to damage in APTX deficient cells.Scientific reports · 2015Article
- Molecular underpinnings of Aprataxin RNA/DNA deadenylase function and dysfunction in neurological disease.Progress in biophysics and molecular biology · 2015Review
- Complementation of aprataxin deficiency by base excision repair enzymes.Nucleic acids research · 2015Article
- Expression of a pathogenic mutation of SOD1 sensitizes aprataxin-deficient cells and mice to oxidative stress and triggers hallmarks of premature ageing.Human molecular genetics · 2015Article
- Recognition and repair of chemically heterogeneous structures at DNA ends.Environmental and molecular mutagenesis · 2015Review
- Role of polymerase β in complementing aprataxin deficiency during abasic-site base excision repair.Nature structural & molecular biology · 2014Article
- Article
- Repair of double-strand breaks by end joining.Cold Spring Harbor perspectives in biology · 2013Review
- Review
- Evidence for abasic site sugar phosphate-mediated cytotoxicity in alkylating agent treated Saccharomyces cerevisiae.PloS one · 2012Article
- Structure of an aprataxin-DNA complex with insights into AOA1 neurodegenerative disease.Nature structural & molecular biology · 2011Article
- To live or to die: a matter of processing damaged DNA termini in neurons.EMBO molecular medicine · 2011Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in Aprataxin cause the neurodegenerative syndrome ataxia oculomotor apraxia type 1. Aprataxin catalyzes removal of adenosine monophosphate (AMP) from the 5' end of a DNA strand, which results from an aborted attempt to ligate a strand break containing a damaged end. To gain insight into which DNA lesions are substrates for Aprataxin action in vivo, we deleted the Saccharomyces cerevisiae HNT3 gene, which encodes the Aprataxin homolog, in combination with known DNA repair genes. While hnt3Delta single mutants were not sensitive to DNA damaging agents, loss of HNT3 caused synergistic sensitivity to H(2)O(2) in backgrounds that accumulate strand breaks with blocked termini, including apn1Delta apn2Delta tpp1Delta and ntg1Delta ntg2Delta ogg1Delta. Loss of HNT3 in rad27Delta cells, which are deficient in long-patch base excision repair (LP-BER), resulted in synergistic sensitivity to H(2)O(2) and MMS, indicating that Hnt3 and LP-BER provide parallel pathways for processing 5' AMPs. Loss of HNT3 also increased the sister chromatid exchange frequency. Surprisingly, HNT3 deletion partially rescued H(2)O(2) sensitivity in recombination-deficient rad51Delta and rad52Delta cells, suggesting that Hnt3 promotes formation of a repair intermediate that is resolved by recombination.
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Registered trials
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