ArticleNature structural & molecular biology2015
CtIP tetramer assembly is required for DNA-end resection and repair.
Article in Nature structural & molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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52 citing papers in PubMed, 74 citations in OpenAlex.
- Pathogenic variants in the human TONSL protein associated with SPONASTRIME dysplasia impair protein dimerization and DNA repair.Science advances · 2026Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- The PIN1-p38-CtIP signalling axis protects stalled replication forks from deleterious degradation.Nucleic acids research · 2025Article
- DNA binding and bridging by human CtIP in the healthy and diseased states.Nucleic acids research · 2024Article
- MEILB2-BRME1 forms a V-shaped DNA clamp upon BRCA2-binding in meiotic recombination.Nature communications · 2024Article
- New Discoveries on Protein Recruitment and Regulation during the Early Stages of the DNA Damage Response Pathways.International journal of molecular sciences · 2024Review
- Recurrence mutation in RBBP8 gene causing non-syndromic autosomal recessive primary microcephaly; geometric simulation approach for insight into predicted computational models.Journal of human genetics · 2023Article
- Differential expression of DNA damage repair genes after chemoradiotherapy and inhibition rate in different bladder cancer cells.Translational andrology and urology · 2022Article
- RNAi Screening Uncovers a Synthetic Sick Interaction between CtIP and the BARD1 Tumor Suppressor.Cells · 2022Article
- The high toxicity of DSB-clusters modelling high-LET-DNA damage derives from inhibition of c-NHEJ and promotion of alt-EJ and SSA despite increases in HR.Frontiers in cell and developmental biology · 2022Article
- p85β alters response to EGFR inhibitor in ovarian cancer through p38 MAPK-mediated regulation of DNA repair.Neoplasia (New York, N.Y.) · 2021Article
- Structural basis for the coiled-coil architecture of human CtIP.Open biology · 2021Article
- Stereo- and regiodefined DNA-encoded chemical libraries enable efficient tumour-targeting applications.Nature chemistry · 2021Article
- A conserved Ctp1/CtIP C-terminal peptide stimulates Mre11 endonuclease activity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A stapled peptide mimetic of the CtIP tetramerization motif interferes with double-strand break repair and replication fork protection.Science advances · 2021Article
- SUMOylation mediates CtIP's functions in DNA end resection and replication fork protection.Nucleic acids research · 2021Article
- Multiple DSB Resection Activities Redundantly Promote Alternative End Joining-Mediated Class Switch Recombination.Frontiers in cell and developmental biology · 2021Article
- CtIP-mediated DNA resection is dispensable for IgH class switch recombination by alternative end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Phosphorylated CtIP bridges DNA to promote annealing of broken ends.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The internal region of CtIP negatively regulates DNA end resection.Nucleic acids research · 2020Article
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11 authors at 1 institution in 1 country.
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Abstract
Mammalian CtIP protein has major roles in DNA double-strand break (DSB) repair. Although it is well established that CtIP promotes DNA-end resection in preparation for homology-dependent DSB repair, the molecular basis for this function has remained unknown. Here we show by biophysical and X-ray crystallographic analyses that the N-terminal domain of human CtIP exists as a stable homotetramer. Tetramerization results from interlocking interactions between the N-terminal extensions of CtIP's coiled-coil region, which lead to a 'dimer-of-dimers' architecture. Through interrogation of the CtIP structure, we identify a point mutation that abolishes tetramerization of the N-terminal domain while preserving dimerization in vitro. Notably, we establish that this mutation abrogates CtIP oligomer assembly in cells, thus leading to strong defects in DNA-end resection and gene conversion. These findings indicate that the CtIP tetramer architecture described here is essential for effective DSB repair by homologous recombination.
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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.