ArticleProceedings of the National Academy of Sciences of the United States of America2021
DNA damage-induced phosphorylation of CtIP at a conserved ATM/ATR site T855 promotes lymphomagenesis in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- Visualization and quantification of rDNA instabilities in mammalian cells and mouse models.Nucleic acids research · 2026Article
- Histone H2A variants play a key role at DNA double-strand breaks during repair pathway choice.Frontiers in epigenetics and epigenomics · 2024Review
- Key molecular DNA damage responses of human cells to radiation.Frontiers in cell and developmental biology · 2024Review
- Combined strategies with PARP inhibitors for the treatment of BRCA wide type cancer.Frontiers in oncology · 2024Review
- Article
- Inactive PARP1 causes embryonic lethality and genome instability in a dominant-negative manner.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion.Nature communications · 2023Article
- Contribution of Microhomology to Genome Instability: Connection between DNA Repair and Replication Stress.International journal of molecular sciences · 2022Review
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
CtIP is a DNA end resection factor widely implicated in alternative end-joining (A-EJ)-mediated translocations in cell-based reporter systems. To address the physiological role of CtIP, an essential gene, in translocation-mediated lymphomagenesis, we introduced the T855A mutation at murine CtIP to nonhomologous end-joining and Tp53 double-deficient mice that routinely succumbed to lymphomas carrying A-EJ-mediated IgH-Myc translocations. T855 of CtIP is phosphorylated by ATM or ATR kinases upon DNA damage to promote end resection. Here, we reported that the T855A mutation of CtIP compromised the neonatal development of
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