Regulation of cellular senescence by p53
Open accessAbstract
Many normal cells respond to potentially oncogenic stimuli by undergoing cellular senescence, a state of irreversibly arrested proliferation and altered differentiated function. Cellular senescence very likely evolved to suppress tumorigenesis. In support of this idea, it is regulated by several tumor suppressor genes. At the heart of this regulation is p53. p53 is essential for the senescence response to short telomeres, DNA damage, oncogenes and supraphysiological mitogenic signals, and overexpression of certain tumor suppressor genes. Despite the well-documented central role for p53 in the senescence response, many questions remain regarding how p53 senses senescence-inducing stimuli and how it elicits the senescent phenotype.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Loss of p53 function delays or abrogates the replicative senescence of human cells.
“It is well established that loss of p53 function delays or abrogates the replicative senescence of human cells (Itahana et al., 2001).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Itahana et al., 2001
The Replicative senescence section says that p53 inactivation extends the replicative lifespan of human cells, supporting a delay. It explicitly says p53 inactivation “delays, but does not abrogate, replicative senescence,” so the abrogation alternative is not supported. (LLM, conf=0.92)
Experimental — accuracy not yet measuredDysfunctional 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 Itahana et al., 2001
The Abstract says p53 is essential for senescence in response to short telomeres. In “How does p53 sense senescence signals?”, the paper suggests that ATM transmits dysfunctional-telomere signals through p53 and notes that DNA-repair proteins associate with telomeres. It does not establish that dysfunctional telomeres activate many components of the p53-mediated damage response; it also distinguishes p53 phosphorylation in senescent cells from that in DNA-damaged cells. No page number is available for these passages in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 84 · Cited by 365
Research works printed but not linked: 1
- Chang, B.D., Watanabe, K., Broude, E.V., Fang, J., Poole, J.C., Kalinichenko, T.V. & Roninson, I.B. (2000) Effects of p21Waf1/ Cip1/Sdi1 on cellular gene expression: implications for carcino- genesis, senescence, and age-related diseases. Proc. Natl Acad. Sci. USA 97, 4291±4296. q FEBS 2001 p53 and cellular senescence (Eur. J. Biochem. 268) 2791 14321033, 2001, 10, Downloaded from https://febs.onlinelibrary.wiley.com/doi/10.1046/j.1432-1327.2001.02228.x, Wiley Online Library on [06/09/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
- Authors
- Itahana, K., Dimri, G., & Campisi, J.
- Affiliations
- Lawrence Berkeley National Laboratory (US)
- Tufts Medical Center (US)
- Venue
- European Journal of Biochemistry
- Publisher
- Wiley
- Published
- 2001-05-15
- Volume
- 268
- Issue
- 10
- Pages
- 2784-2791
- ISSN
- 0014-2956 (ISSN-L)
- 1432-1033
- OpenAlex
- W1523325879
- Cited by
- 365
- References
- 84
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 4 · 2023: 10 · 2022: 5 · 2021: 15 · 2020: 6 · 2019: 5 · 2018: 15 · 2017: 11 · 2016: 16 · 2015: 23 · 2014: 15 · 2013: 15 · 2012: 21
- FWCI
- 3.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, p53, tumor suppressor, telomere shortening, DNA damage response, oncogene-induced senescence, mitogenic signaling, senescence-associated phenotype, tumorigenesis suppression
- MeSH terms
- Aging, Animals, Cell Division, DNA Damage, Humans, Models, Biological, Neoplasms, Phenotype, Signal Transduction, Tumor Suppressor Protein p53, Telomere
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
