ArticleThe EMBO journal2015
BRCA1 and CtIP promote alternative non-homologous end-joining at uncapped telomeres.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026Review
- Review
- Fanconi anemia and dyskeratosis congenita/telomere biology disorders: Two inherited bone marrow failure syndromes with genomic instability.Frontiers in oncology · 2022Review
- Measuring nonhomologous end-joining, homologous recombination and alternative end-joining simultaneously at an endogenous locus in any transfectable human cell.Nucleic acids research · 2021Article
- XRCC1 promotes replication restart, nascent fork degradation and mutagenic DNA repair in BRCA2-deficient cells.NAR cancer · 2020Article
- An Integrative Omics Approach Reveals Involvement ofCancers · 2020Article
- Both the classical and alternative non-homologous end joining pathways contribute to the fusion of drastically shortened telomeres induced by TRF2 overexpression.Cell cycle (Georgetown, Tex.) · 2019Article
- BRCA1 ensures genome integrity by eliminating estrogen-induced pathological topoisomerase II-DNA complexes.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Werner Syndrome Protein and DNA Replication.International journal of molecular sciences · 2018Review
- PARP1 is required for preserving telomeric integrity but is dispensable for A-NHEJ.Oncotarget · 2018Article
- Tankyrase1-mediated poly(ADP-ribosyl)ation of TRF1 maintains cell survival after telomeric DNA damage.Nucleic acids research · 2017Article
- Microhomology-mediated end joining induces hypermutagenesis at breakpoint junctions.PLoS genetics · 2017Article
- Differences in the recruitment of DNA repair proteins at subtelomeric and interstitial I-SceI endonuclease-induced DNA double-strand breaks.DNA repair · 2017Article
- WRN regulates pathway choice between classical and alternative non-homologous end joining.Nature communications · 2016Article
- Unsolved mystery: the role of BRCA1 in DNA end-joining.Journal of radiation research · 2016Review
- A role for human homologous recombination factors in suppressing microhomology-mediated end joining.Nucleic acids research · 2016Article
- Stop pulling my strings - what telomeres taught us about the DNA damage response.Nature reviews. Molecular cell biology · 2016Review
- The DNA resection protein CtIP promotes mammary tumorigenesis.Oncotarget · 2016Article
- TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions.Nature communications · 2016Article
- DNA repair factor BRCA1 depletion occurs in Alzheimer brains and impairs cognitive function in mice.Nature communications · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Loss of telomere protection occurs during physiological cell senescence and ageing, due to attrition of telomeric repeats and insufficient retention of the telomere-binding factor TRF2. Subsequently formed telomere fusions trigger rampant genomic instability leading to cell death or tumorigenesis. Mechanistically, telomere fusions require either the classical non-homologous end-joining (C-NHEJ) pathway dependent on Ku70/80 and LIG4, or the alternative non-homologous end-joining (A-NHEJ), which relies on PARP1 and LIG3. Here, we show that the tumour suppressor BRCA1, together with its interacting partner CtIP, both acting in end resection, also promotes end-joining of uncapped telomeres. BRCA1 and CtIP do not function in the ATM-dependent telomere damage signalling, nor in telomere overhang removal, which are critical for telomere fusions by C-NHEJ. Instead, BRCA1 and CtIP act in the same pathway as LIG3 to promote joining of de-protected telomeres by A-NHEJ. Our work therefore ascribes novel roles for BRCA1 and CtIP in end-processing and fusion reactions at uncapped telomeres, underlining the complexity of DNA repair pathways that act at chromosome ends lacking protective structures. Moreover, A-NHEJ provides a mechanism of previously unanticipated significance in telomere dysfunction-induced genome instability.
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What OpenQuestion holds
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.