ArticleNucleic acids research2019
CtIP is essential for telomere replication.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
The trial behind it
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
9 citing papers in PubMed, 15 citations in OpenAlex.
- A novel RBBP8(p.E281*) germline mutation is a predisposing mutation in familial hereditary cancer syndrome.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Interactions between the DNA Damage Response and the Telomere Complex in Carcinogenesis: A Hypothesis.Current issues in molecular biology · 2023Review
- Kinome-wide screening uncovers a role for Bromodomain Protein 3 in DNA double-stranded break repair.DNA repair · 2023Article
- Review
- Homologous recombination within repetitive DNA.Current opinion in genetics & development · 2021Review
- To Join or Not to Join: Decision Points Along the Pathway to Double-Strand Break Repair vs. Chromosome End Protection.Frontiers in cell and developmental biology · 2021Review
- Extrachromosomal Circular DNA: Current Knowledge and Implications for CNS Aging and Neurodegeneration.International journal of molecular sciences · 2020Review
- Telomere fusions and translocations: a bridge too far?Current opinion in genetics & development · 2020Review
- Replication Stress at Telomeric and Mitochondrial DNA: Common Origins and Consequences on Ageing.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The maintenance of telomere length is critical to longevity and survival. Specifically, the failure to properly replicate, resect, and/or form appropriate telomeric structures drives telomere shortening and, in turn, genomic instability. The endonuclease CtIP is a DNA repair protein that is well-known to promote genome stability through the resection of endogenous DNA double-stranded breaks. Here, we describe a novel role for CtIP. We show that in the absence of CtIP, human telomeres shorten rapidly to non-viable lengths. This telomere dysfunction results in an accumulation of fusions, breaks, and frank telomere loss. Additionally, CtIP suppresses the generation of circular, extrachromosomal telomeric DNA. These latter structures appear to arise from arrested DNA replication forks that accumulate in the absence of CtIP. Hence, CtIP is required for faithful replication through telomeres via its roles at stalled replication tracts. Our findings demonstrate a new role for CtIP as a protector of human telomere integrity.
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Registered trials
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.