ArticleNature cell biology2010
Positive feedback between p53 and TRF2 during telomere-damage signalling and cellular senescence.
Article in Nature cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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.
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Who cites it
69 citing papers in PubMed, 101 citations in OpenAlex.
- TRF2 couples muscle stem cell identity to regenerative repair.Science advances · 2026Article
- Telomere biology and telomerase regulation across species: evolutionary insights into aging, longevity, and genome stability.Molecular biology reports · 2026Review
- Microgravity Impacts the Expression of Aging-Associated Candidate Gene Targets in the p53 Regulatory Network.International journal of molecular sciences · 2025Article
- Telomeres control human telomerase (eLife · 2025Article
- hTERT Increases TRF2 to Induce Telomere Compaction and Extend Cell Replicative Lifespan.Aging cell · 2025Article
- Causality of Aging Hallmarks.Aging and disease · 2025Review
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- IRF3 activates RB to authorize cGAS-STING-induced senescence and mitigate liver fibrosis.Science advances · 2024Article
- Paeonol Attenuates Atherosclerosis by Inhibiting Vascular Smooth Muscle Cells Senescence via SIRT1/P53/TRF2 Signaling Pathway.Molecules (Basel, Switzerland) · 2024Article
- Ginsenoside F1-Mediated Telomere Preservation Delays Cellular Senescence.International journal of molecular sciences · 2023Article
- EPAS1 prevents telomeric damage-induced senescence by enhancing transcription ofZoological research · 2023Article
- The Imbalance of p53-Park7 Signaling Axis Induces Iron Homeostasis Dysfunction in Doxorubicin-Challenged Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Senescence-associated transcriptional derepression in subtelomeres is determined in a chromosome-end-specific manner.Aging cell · 2023Article
- Aberrant expression and localization of the RAP1 shelterin protein contribute to age-related phenotypes.PLoS genetics · 2022Article
- SIAH1-mediated RPS3 ubiquitination contributes to chemosensitivity in epithelial ovarian cancer.Aging · 2022Article
- Selective pericentromeric heterochromatin dismantling caused by TP53 activation during senescence.Nucleic acids research · 2022Article
- TRF2 inhibition rather than telomerase disruption drives CD4T cell dysfunction during chronic viral infection.Journal of cell science · 2022Article
- Article
- Reactive oxygen species-induced SIAH1 promotes granulosa cells' senescence in premature ovarian failure.Journal of cellular and molecular medicine · 2022Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 4 countries.
Funding
Abstract
The telomere-capping complex shelterin protects functional telomeres and prevents the initiation of unwanted DNA-damage-response pathways. At the end of cellular replicative lifespan, uncapped telomeres lose this protective mechanism and DNA-damage signalling pathways are triggered that activate p53 and thereby induce replicative senescence. Here, we identify a signalling pathway involving p53, Siah1 (a p53-inducible E3 ubiquitin ligase) and TRF2 (telomere repeat binding factor 2; a component of the shelterin complex). Endogenous Siah1 and TRF2 were upregulated and downregulated, respectively, during replicative senescence with activated p53. Experimental manipulation of p53 expression demonstrated that p53 induces Siah1 and represses TRF2 protein levels. The p53-dependent ubiquitylation and proteasomal degradation of TRF2 are attributed to the E3 ligase activity of Siah1. Knockdown of Siah1 stabilized TRF2 and delayed the onset of cellular replicative senescence, suggesting a role for Siah1 and TRF2 in p53-regulated senescence. This study reveals that p53, a downstream effector of telomere-initiated damage signalling, also functions upstream of the shelterin complex.
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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.