The DOI matches its Crossref record; 165 of the 167 references it cites were found in a registry or an index.
Coping with stress: multiple ways to activate p53
Abstract
Over the years, p53 has been shown to sit at the centre of an increasingly complex web of incoming stress signals and outgoing effector pathways. The number and diversity of stress signals that lead to p53 activation illustrates the breadth of p53's remit - responding to a wide variety of potentially oncogenic insults to prevent tumour development. Interestingly, different stress signals can use different and independent pathways to activate p53, and there is some evidence that different stress signals can mediate different responses. How each of the responses to p53 contributes to inhibition of malignant progression is beginning to be clarified, with the hope that identification of responses that are key to tumour suppression will allow a more focused and effective search for new therapeutic targets. In this review, we will highlight some recently identified roles for p53 in tumour suppression, and discuss some of the numerous mechanisms through which p53 can be regulated and activated.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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?
In the citing paper
“p53 is activated in response to stress signals—DNA damage, oncogene activation, ribosomal stress and hypoxia4 —and leads to growth suppression by inducing cell cycle arrest or cell death.”
From Census and evaluation of p53 target genes (2017) · cites this paper as [4]
Citations
Cites
1 retracted
RETRACTED: The E3 SUMO Ligase PIASy Is a Regulator of Cellular Senescence and Apoptosis
Bischof, O., Schwamborn, K., Martin, N., Werner, A., Sustmann, C., Grosschedl, R., & Dejean, A. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.05.016 · Cited by 172
RetractedVogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 1×
“The p53 protein is a transcription factor that regulates the expression of a large number of target genes (Vogelstein et al., 2000).”
BackgroundCDK inhibitors: positive and negative regulators of G1-phase progression
Sherr, C. J., & Roberts, J. M. (1999) · Genes & Development · doi:10.1101/gad.13.12.1501 · Cited by 6,115
The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis
Maxwell, P. H., Wiesener, M. S., Chang, G.-W., Clifford, S. C., Vaux, E. C., Cockman, M. E., Wykoff, C. C., Pugh, C. W., Maher, E. R., & Ratcliffe, P. J. (1999) · Nature · doi:10.1038/20459 · Cited by 5,180
In Vivo Activation of the p53 Pathway by Small-Molecule Antagonists of MDM2
Vassilev, L. T., Vu, B. T., Graves, B., Carvajal, D., Podlaski, F., Filipovic, Z., Kong, N., Kammlott, U., Lukacs, C., Klein, C., et al. (2004) · Science · doi:10.1126/science.1092472 · Cited by 4,661
Danial, N. N., & Korsmeyer, S. J. (2004) · Cell · doi:10.1016/s0092-8674(04)00046-7 · Cited by 4,651
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Germ Line p53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms
Malkin, D., Li, F. P., Strong, L. C., Fraumeni, J. F., Nelson, C. E., Kim, D. H., Kassel, J., Gryka, M. A., Bischoff, F. Z., Tainsky, M. A., et al. (1990) · Science · doi:10.1126/science.1978757 · Cited by 3,765
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
Bartkova, J., Hořejší, Z., Koed, K., Krämer, A., Tort, F., Zieger, K., Guldberg, P., Sehested, M., Nesland, J. M., Lukas, C., et al. (2005) · Nature · doi:10.1038/nature03482 · Cited by 2,688
PUMA, a Novel Proapoptotic Gene, Is Induced by p53
Nakano, K., & Vousden, K. H. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00214-3 · Cited by 2,315
Self-citation
Cited by
Sorted by citations
Items 501–524 of 524
Tavernarakis, N., & Markaki, M. (2010) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.3620956.6935058
Non-canonical functions of the MDM2 oncoprotein
Manzini, V. (2022) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-9537
Stieg, D. C., Parris, J. L. D., Yang, T. H. L., Mirji, G., Reiser, S. K., Murali, N., Werts, M., Barnoud, T., Lu, D. Y., Shinde, R. S., et al. (2023) · doi:10.1158/2767-9764.c.6702845
Hofseth, L. J., Weston, A., & Harris, C. C. (2017) · Wiley eBooks · doi:10.1002/9781119000822.hfcm023
Perez, M. (2024) · FIU Undergraduate Research Journal · doi:10.25148/urj.020118
Das Onkoprotein Mdm4 und seine Wirkung auf die DNA-Replikation
Wohlberedt, K. (2024) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-10645
Exploring the impact of p53 activation on spatio-temporal genome topology
Pasadas, M. C. (2024) · UPCommons institutional repository (Universitat Politècnica de Catalunya) · doi:10.5821/dissertation-2117-422069
Stubbe, M., Stubbe, H. C., Mai, J., Plank, V., Hofmann, S., Göttig, L., Günther, T., Grundhoff, A. T., Krebs, S., Groitl, P., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.02.07.636424
The Cell Cycle in Cancer: Molecular Pathways, Checkpoint Aberrations, and Therapeutic Opportunities
Zalli, D., & Gabrani, J. (2025) · Medicus · doi:10.58944/ycfe5589
Does loss of PRH alter the sensitivity of Dasatinib in breast tumour cells
ماوی, ن. ک. (2015) · University of Birmingham Institutional Research Archive (University of Birmingham)
Hänze, J., Mengen, L. M., Mernberger, M., Tiwari, D. K., Plagge, T., Nist, A., Subtil, F. S. B., Theiß, U., Eberle, F., Roth, K., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26741942
Le récepteur orphelin GPR158 : fonction et partenaires protéiques
Hajj, M. (2012) · theses.fr (ABES) · doi:10.70675/e75ab04fzf6ddz4c25zb55dz5eefb493d85c
Impact de l’autophagie sur la radiosensibilité tumorale
Ko, A. (2013) · theses.fr (ABES) · doi:10.70675/bb8f00d2ze478z4bbcz883aze4a06af07318
Factors That Affect Chromosomal Translocations in Cells
Canoy, R. J. (2021) · theses.fr (ABES) · doi:10.70675/9f331f7az9151z4c95zbf47zbc6ed65a5896
Masoodi, G., Sofi, S., Jan, N., & Mir, M. A. (2026) · Results in Chemistry · doi:10.1016/j.rechem.2026.103409
Ohbayashi, I., Hsu, T.-Y., Faustine, J., Chiang, P.-C., Miyashita, T., Yonekura, T., Iwamoto, A., Furutani, M., & Sugiyama, M. (2026) · Plant and Cell Physiology · doi:10.1093/pcp/pcag096
Li, J., Huang, H., Wang, M., & Hang, Q. (2026) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2026.189724
The ubiquitin ligase G2E3 modulates cell proliferation, survival and the DNA damage response
Schmidt, F. (2014) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-4625
DNA damage recognition in the normal epithelium of human prostate and seminal vesicles
Jäämaa, S. (2011) · Työväentutkimus Vuosikirja
Metadata
- Authors
- Horn, H. F., & Vousden, K. H.
- Affiliations
- Cancer Research UK Scotland Institute (GB)
- Corresponding author
- Vousden, K H
- Venue
- Oncogene
- Published
- 2007-02-26
- Volume
- 26
- Issue
- 9
- Pages
- 1306-1316
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2035188342
- Semantic Scholar
- ea46e0441d9175c80c0ddbd29c6fc13c60a82939
- Cited by
- 522
- References
- 167
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 18 · 2023: 22 · 2022: 20 · 2021: 30 · 2020: 23 · 2019: 27 · 2018: 35 · 2017: 37 · 2016: 35 · 2015: 30 · 2014: 26 · 2013: 36 · 2012: 26
- FWCI
- 3.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- p53, stress signals, p53 activation, tumor suppression, stress response pathways, malignant progression, therapeutic target
- MeSH terms
- Humans, Neoplasms, Signal Transduction, Tumor Suppressor Protein p53, Oxidative Stress
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
