Functional links between telomeres and proteins of the DNA-damage response
Open accessAbstract
In response to DNA damage, cells engage a complex set of events that together comprise the DNA-damage response (DDR). These events bring about the repair of the damage and also slow down or halt cell cycle progression until the damage has been removed. In stark contrast, the ends of linear chromosomes, telomeres, are generally not perceived as DNA damage by the cell even though they terminate the DNA double-helix. Nevertheless, it has become clear over the past few years that many proteins involved in the DDR, particularly those involved in responding to DNA double-strand breaks, also play key roles in telomere maintenance. In this review, we discuss the current knowledge of both the telomere and the DDR, and then propose an integrated model for the events associated with the metabolism of DNA ends in these two distinct physiological contexts.
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Dysfunctional telomeres activate many components of the p53-mediated damage response, and the senescence response to dysfunctional telomeres requires integrity of the p53 pathway.
“Moreover, dysfunctional telomeres activate many components of the p53-mediated damage response, and the senescence response to dysfunctional telomeres requires integrity of the p53 pathway (Itahana et al., 2001; d’Adda di Fagagna et al., 2004).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as d’Adda di Fagagna et al., 2004
In “DDR proteins at dysfunctional telomeres” (page unavailable), the review says critically short telomeres activate multiple DNA-damage checkpoint components and that interfering with checkpoint kinases allows some senescent cells to resume cycling. Its references also name a study of telomere-shortening-induced senescence through a pathway involving ATM, p53, and p21. The review does not itself establish the stronger claim that the senescence response requires an intact p53 pathway. (LLM, conf=0.82)
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References 196 · Cited by 277
Research works printed but not linked: 1
- Karnitz, L.M. 2004. Dial 9-1-1 for DNA damage: The Rad9- Hus1-Rad1 clamp complex. DNA Repair (Amst.) (in press).
- Authors
- d'Adda di Fagagna, F., Teo, S.-H., & Jackson, S. P.
- Affiliations
- University of Cambridge (GB)
- ORCID
- Teo, Soo-Hwang
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2004-08-01
- Volume
- 18
- Issue
- 15
- Pages
- 1781-1799
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2149129068
- Cited by
- 277
- References
- 196
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 3 · 2023: 12 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 3 · 2018: 11 · 2017: 8 · 2016: 5 · 2015: 10 · 2014: 14 · 2013: 9 · 2012: 19
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Cancer Research UK
- European Commission
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- telomeres, DNA damage response, telomere maintenance, DNA double-strand breaks, chromosome ends, cell cycle checkpoints, DNA repair
- MeSH terms
- Animals, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, Humans, Nuclear Proteins, Telomere
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