ArticleNucleic acids research2017
Tankyrase1-mediated poly(ADP-ribosyl)ation of TRF1 maintains cell survival after telomeric DNA damage.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Loci for human leukocyte telomere length in the Singaporean Chinese population and trans-ethnic genetic studies.Nature communications · 2019Pooled it
- Tankyrase activity is essential for asymmetric division and chromosome segregation in oocyte meiosis.Journal of advanced research · 2026Article
- PARylation-centric crosstalk: orchestrating immune evasion and multidrug resistance in ovarian cancer.Frontiers in immunology · 2026Review
- Understanding Tankyrase Inhibitors and Their Role in the Management of Different Cancer.Current cancer drug targets · 2025Review
- RNF166 promotes colorectal cancer progression by recognizing and destabilizing poly-ADP-ribosylated angiomotins.Cell death & disease · 2024Article
- Unravelling the Structural Mechanism of Action of 5-methyl-5-[4-(4-oxo-3H-quinazolin-2-yl)phenyl]imidazolidine-2,4-dione in Dual-Targeting Tankyrase 1 and 2: A Novel Avenue in Cancer Therapy.Cell biochemistry and biophysics · 2022Article
- Knockdown of tankyrase 1 inhibits the progression of gastric adenocarcinoma via regulating human telomerase reverse transcriptase and telomeric repeat binding factor 1.Journal of gastrointestinal oncology · 2022Article
- Functions of ADP-ribose transferases in the maintenance of telomere integrity.Cellular and molecular life sciences : CMLS · 2022Review
- Functional roles of ADP-ribosylation writers, readers and erasers.Frontiers in cell and developmental biology · 2022Review
- Review
- Tankyrases as modulators of pro-tumoral functions: molecular insights and therapeutic opportunities.Journal of experimental & clinical cancer research : CR · 2021Review
- Review
- Dynamics of TRF1 organizing a single human telomere.Nucleic acids research · 2021Article
- DNA damage and mitochondria in cancer and aging.Carcinogenesis · 2020Review
- Nuclear PARPs and genome integrity.Genes & development · 2020Review
- An R-loop-initiated CSB-RAD52-POLD3 pathway suppresses ROS-induced telomeric DNA breaks.Nucleic acids research · 2020Article
- Poly(ADP-ribose) polymerase enzymes and the maintenance of genome integrity.Cellular and molecular life sciences : CMLS · 2020Review
- Stilbene Compounds Inhibit Tumor Growth by the Induction of Cellular Senescence and the Inhibition of Telomerase Activity.International journal of molecular sciences · 2019Review
- Emerging roles of eraser enzymes in the dynamic control of protein ADP-ribosylation.Nature communications · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Oxidative DNA damage triggers telomere erosion and cellular senescence. However, how repair is initiated at telomeres is largely unknown. Here, we found unlike PARP1-mediated Poly-ADP-Ribosylation (PARylation) at genomic damage sites, PARylation at telomeres is mainly dependent on tankyrase1 (TNKS1). TNKS1 is recruited to damaged telomeres via its interaction with TRF1, which subsequently facilitates the PARylation of TRF1 after damage. TNKS inhibition abolishes the recruitment of the repair proteins XRCC1 and polymerase β at damaged telomeres, while the PARP1/2 inhibitor only has such an effect at non-telomeric damage sites. The ANK domain of TNKS1 is essential for the telomeric damage response and TRF1 interaction. Mutation of the tankyrase-binding motif (TBM) on TRF1 (13R/18G to AA) disrupts its interaction with TNKS1 concomitant recruitment of TNKS1 and repair proteins after damage. Either TNKS1 inhibition or TBM mutated TRF1 expression markedly sensitizes cells to telomere oxidative damage as well as XRCC1 inhibition. Together, our data reveal a novel role of TNKS1 in facilitating SSBR at damaged telomeres through PARylation of TRF1, thereby protecting genome stability and cell viability.
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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.