ArticleNucleus (Austin, Tex.)2015
When two is not enough: a CtIP tetramer is required for DNA repair by Homologous Recombination.
Article in Nucleus (Austin, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- A stapled peptide mimetic of the CtIP tetramerization motif interferes with double-strand break repair and replication fork protection.Science advances · 2021Article
- Extending the scope of coiled-coil crystal structure solution by AMPLE through improved ab initio modelling.Acta crystallographica. Section D, Structural biology · 2020Article
- CtIP is essential for early B cell proliferation and development in mice.The Journal of experimental medicine · 2019Article
- Article
- CtIP/Ctp1/Sae2, molecular form fit for function.DNA repair · 2017Review
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Homologous recombination (HR) is central to the repair of double-strand DNA breaks that occur in S/G2 phases of the cell cycle. HR relies on the CtIP protein (Ctp1 in fission yeast, Sae2 in budding yeast) for resection of DNA ends, a key step in generating the 3'-DNA overhangs that are required for the HR strand-exchange reaction. Although much has been learned about the biological importance of CtIP in DNA repair, our mechanistic insight into its molecular functions remains incomplete. It has been recently discovered that CtIP and Ctp1 share a conserved tetrameric architecture that is mediated by their N-terminal domains and is critical for their function in HR. The specific arrangement of protein chains in the CtIP/Ctp1 tetramer indicates that an ability to bridge DNA ends might be an important feature of CtIP/Ctp1 function, establishing an intriguing similarity with the known ability of the MRE11-RAD50-NBS1 complex to link DNA ends. Although the exact mechanism of action remains to be elucidated, the remarkable evolutionary conservation of CtIP/Ctp1 tetramerisation clearly points to its crucial role in HR.
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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.