The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Increased p53 activity does not accelerate telomere‐driven ageing
Open accessAbstract
There is a great interest in determining the impact of p53 on ageing and, for this, it is important to discriminate among the known causes of ageing. Telomere loss is a well-established source of age-associated damage, which by itself can recapitulate ageing in mouse models. Here, we have used a genetic approach to interrogate whether p53 contributes to the elimination of telomere-damaged cells and its impact on telomere-driven ageing. We have generated compound mice carrying three functional copies of the p53 gene (super-p53) in a telomerase-deficient background and we have measured the presence of chromosomal abnormalities and DNA damage in several tissues. We have found that the in vivo load of telomere-derived chromosomal damage is significantly decreased in super-p53/telomerase-null mice compared with normal-p53/telomerase-null mice. Interestingly, the presence of extra p53 activity neither accelerates nor delays telomere-driven ageing. From these observations, we conclude that p53 has an active role in eliminating telomere-damaged cells, and we exclude the possibility of an age-promoting effect of p53 on telomere-driven ageing.
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“recent evidence suggest that mouse telomeres suffer a dramatic shortening at old ages and that telomere length can be rate-limiting for mouse longevity (Flores et al, 2008; Garcia-Cao et al, 2006).”
From Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer (2012) · cites this paper as Garcia-Cao et al, 2006
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“Telomerase also acts as a longevity gene in the context of the organism by preventing premature telomere attrition, as illustrated by both telomerase-deficient mice and by human diseases due to mutations in telomerase components, which suffer from premature adult stem cell dysfunction and decreased longevity due to accelerated rates of telomere shortening even at the first generation (Armanios et”
From Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer (2012) · cites this paper as Garcia-Cao et al, 2006
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“recent evidence suggest that mouse telomeres suffer a dramatic shortening at old ages and that telomere length can be rate-limiting for mouse longevity (Flores et al, 2008; Garcia-Cao et al, 2006).”
From Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer (2012) · cites this paper as Garcia-Cao et al, 2006
In the citing paper
“First generation mice lacking the telomerase RNA component Terc show a decrease in both their median and maximum lifespan, and these effects become more pronounced with each subsequent generation 65 .”
From The common biology of cancer and ageing (2007) · cites this paper as [65]
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Citations
Cites
A DNA damage checkpoint response in telomere-initiated senescence
Fagagna, F. D. D., Reaper, P. M., Clay-Farrace, L., Fiegler, H., Carr, P., von Zglinicki, T., Saretzki, G., Carter, N. P., & Jackson, S. P. (2003) · Nature · doi:10.1038/nature02118 · Cited by 2,917 · cited 2×
“Previous investigators have shown that dysfunctional telomeres trigger the formation of g-H2AX foci (d’Adda di Fagagna et al, 2003; Takai et al, 2003; Hao et al, 2004) and, moreover, that there is an age-dependent increase in the number of cells containing g-H2AX foci (Sedelnikova et al, 2004).”
Backgroundp53 is required for radiation-induced apoptosis in mouse thymocytes
Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T. (1993) · Nature · doi:10.1038/362847a0 · Cited by 2,864
Switching and Signaling at the Telomere
Blackburn, E. H. (2001) · Cell · doi:10.1016/s0092-8674(01)00492-5 · Cited by 2,139
Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA
Blasco, M. A., Lee, H.-W., Hande, M. P., Samper, E., Lansdorp, P. M., DePinho, R. A., & Greider, C. W. (1997) · Cell · doi:10.1016/s0092-8674(01)80006-4 · Cited by 2,108
Self-citationAssociation between telomere length in blood and mortality in people aged 60 years or older
Cawthon, R. M., Smith, K. R., O'Brien, E., Sivatchenko, A., & Kerber, R. A. (2003) · The Lancet · doi:10.1016/s0140-6736(03)12384-7 · Cited by 1,761
p53 mutant mice that display early ageing-associated phenotypes
Tyner, S. D., Venkatachalam, S., Choi, J., Jones, S., Ghebranious, N., Igelmann, H., Lu, X., Soron, G., Cooper, B., Brayton, C., et al. (2002) · Nature · doi:10.1038/415045a · Cited by 1,459
DNA Damage Foci at Dysfunctional Telomeres
Takai, H., Smogorzewska, A., & de Lange, T. (2003) · Current Biology · doi:10.1016/s0960-9822(03)00542-6 · Cited by 1,409
Longevity, Stress Response, and Cancer in Aging Telomerase-Deficient Mice
Rudolph, K. L., Chang, S., Lee, H.-W., Blasco, M., Gottlieb, G. J., Greider, C., & DePinho, R. A. (1999) · Cell · doi:10.1016/s0092-8674(00)80580-2 · Cited by 1,349 · cited 2×
“…of telomere dysfunction in somatic cells is a generalized proliferative defect culminating in diverse symptoms of tissue atrophy that become particularly evident in highly proliferative tissues such as the intestine, spleen and testis (Lee et al, 1998; Herrera et al, 1999; Rudolph et al, 1999).”
BackgroundSelf-citationEssential role of mouse telomerase in highly proliferative organs
Lee, H.-W., Blasco, M. A., Gottlieb, G. J., Horner, J. W., Greider, C. W., & DePinho, R. A. (1998) · Nature · doi:10.1038/33345 · Cited by 1,270 · cited 1×
“…of telomere dysfunction in somatic cells is a generalized proliferative defect culminating in diverse symptoms of tissue atrophy that become particularly evident in highly proliferative tissues such as the intestine, spleen and testis (Lee et al, 1998; Herrera et al, 1999; Rudolph et al, 1999).”
BackgroundSelf-citationTelomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice
Artandi, S. E., Chang, S., Lee, S.-L., Alson, S., Gottlieb, G. J., Chin, L., & DePinho, R. A. (2000) · Nature · doi:10.1038/35020592 · Cited by 1,085
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Das, U. N. (2011) · Springer eBooks · doi:10.1007/978-94-007-0495-4_15
37 kDa LRP::FLAG enhances telomerase activity and reduces ageing markers in vivo
Otgaar, T. C., Bernert, M., Morris, G., Baichan, P., Bignoux, M. J., Letsolo, B. T., Weiss, S. F. T., & Ferreira, E. (2025) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-025-05593-0
“Although the dynamic that governs telomere biology in ageing is different between humans and mice, treatments that modulate telom - erase and the telomeres still produce comparable effects, especially for healthier ageing in humans and mice [ 75 , 76 ].”
Metadata
- Authors
- García‐Cao, I., García‐Cao, M., Tomás‐Loba, A., Martin‐Caballero, J., Flores, J. M., Klatt, P., Blasco, M. A., & Serrano, M.
- Affiliations
- Universidad Complutense de Madrid (ES)
- Corresponding author
- Serrano, Manuel
- Venue
- The EMBO Reports
- Published
- 2006-03-31
- Volume
- 7
- Issue
- 5
- Pages
- 546-552
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC1479549
- OpenAlex
- W1979784082
- Cited by
- 102
- References
- 41
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 3 · 2022: 2 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 2 · 2017: 5 · 2016: 5 · 2015: 1 · 2014: 1 · 2013: 4 · 2012: 10
- FWCI
- 8.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- EMBO Reports (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Hispana (submittedVersion, cc-by)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- p53, telomere loss, chromosomal damage, DNA damage, p53 overexpression
- MeSH terms
- Aging, Animals, Kinetics, Mice, Inbred C57BL, Mice, Transgenic, Up-Regulation, Tumor Suppressor Protein p53, Telomere, Mice, Knockout, Gene Dosage, Telomerase, Mice
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