ArticleThe Journal of biological chemistry2017
The non-homologous end-joining factor Nej1 inhibits resection mediated by Dna2-Sgs1 nuclease-helicase at DNA double strand breaks.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Fmp45 promotes Rad53 dephosphorylation via Ptc2 interaction to attenuate checkpoint signaling and maintain genome stability.Journal, genetic engineering & biotechnology · 2025Article
- Nej1 interacts with Sae2 at DNA double-stranded breaks to inhibit DNA resection.The Journal of biological chemistry · 2022Article
- Mapping yeast mitotic 5' resection at base resolution reveals the sequence and positional dependence of nucleases in vivo.Nucleic acids research · 2021Article
- Antagonistic relationship of NuA4 with the non-homologous end-joining machinery at DNA damage sites.PLoS genetics · 2021Article
- Behavior of dicentric chromosomes in budding yeast.PLoS genetics · 2021Article
- A high-throughput alpha particle irradiation system for monitoring DNA damage repair, genome instability and screening in human cell and yeast model systems.Nucleic acids research · 2020Article
- Ku complex suppresses recombination in the absence of MRX activity during budding yeast meiosis.BMB reports · 2019Article
- Nej1 Interacts with Mre11 to Regulate Tethering and Dna2 Binding at DNA Double-Strand Breaks.Cell reports · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Double strand breaks (DSBs) represent highly deleterious DNA damage and need to be accurately repaired. Homology-directed repair and non-homologous end joining (NHEJ) are the two major DSB repair pathways that are highly conserved from yeast to mammals. The choice between these pathways is largely based on 5' to 3' DNA resection, and NHEJ proceeds only if resection has not been initiated. In yeast, yKu70/80 rapidly localizes to the break, protecting DNA ends from nuclease accessibility, and recruits additional NHEJ factors, including Nej1 and Lif1. Cells harboring the
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Registered trials
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