ArticleNucleic acids research2013
Phosphorylated (pT371)TRF1 is recruited to sites of DNA damage to facilitate homologous recombination and checkpoint activation.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- CDK2-mediated phosphorylation of TRF1 S11 facilitates DNA damage repair by remodeling telomeric chromatin.Cell death and differentiation · 2026Article
- Targeting CDK1 in cancer: mechanisms and implications.NPJ precision oncology · 2023Review
- Extracellular Vesicles and Cardiac Aging.Advances in experimental medicine and biology · 2023Article
- Anthracycline-induced cardiotoxicity and cell senescence: new therapeutic option?Cellular and molecular life sciences : CMLS · 2022Review
- RIF1 Links Replication Timing with Fork Reactivation and DNA Double-Strand Break Repair.International journal of molecular sciences · 2021Review
- Telomere-binding proteins Taz1 and Rap1 regulate DSB repair and suppress gross chromosomal rearrangements in fission yeast.PLoS genetics · 2019Article
- Article
- ATM and CDK2 control chromatin remodeler CSB to inhibit RIF1 in DSB repair pathway choice.Nature communications · 2017Article
- Short-term inhibition of TERT induces telomere length-independent cell cycle arrest and apoptotic response in EBV-immortalized and transformed B cells.Cell death & disease · 2016Article
- TRF1 phosphorylation on T271 modulates telomerase-dependent telomere length maintenance as well as the formation of ALT-associated PML bodies.Scientific reports · 2016Article
- Cockayne syndrome group B protein regulates DNA double-strand break repair and checkpoint activation.The EMBO journal · 2015Article
- A primary melanoma and its asynchronous metastasis highlight the role of BRAF, CDKN2A, and TERT.Journal of cutaneous pathology · 2015Article
- 53BP1, BRCA1, and the choice between recombination and end joining at DNA double-strand breaks.Molecular and cellular biology · 2014Review
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5 authors at 1 institution in 1 country.
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Abstract
TRF1, a duplex telomeric DNA-binding protein, plays an important role in telomere metabolism. We have previously reported that a fraction of endogenous TRF1 can stably exist free of telomere chromatin when it is phosphorylated at T371 by Cdk1; however, the role of this telomere-free (pT371)TRF1 has yet to be fully characterized. Here we show that phosphorylated (pT371)TRF1 is recruited to sites of DNA damage, forming damage-induced foci in response to ionizing radiation (IR), etoposide and camptothecin. We find that IR-induced (pT371)TRF1 foci formation is dependent on the ATM- and Mre11/Rad50/Nbs1-mediated DNA damage response. While loss of functional BRCA1 impairs the formation of IR-induced (pT371)TRF1 foci, depletion of either 53BP1 or Rif1 stimulates IR-induced (pT371)TRF1 foci formation. In addition, we show that TRF1 depletion or the lack of its phosphorylation at T371 impairs DNA end resection and repair of nontelomeric DNA double-strand breaks by homologous recombination. The lack of TRF1 phosphorylation at T371 also hampers the activation of the G2/M checkpoint and sensitizes cells to PARP inhibition, IR and camptothecin. Collectively, these results reveal a novel but important function of phosphorylated (pT371)TRF1 in facilitating DNA double-strand break repair and the maintenance of genome integrity.
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