The DOI matches its Crossref record; 231 of the 232 references it cites were found in a registry or an index.
Blinded by the Light: The Growing Complexity of p53
Open accessAbstract
While the tumor suppressor functions of p53 have long been recognized, the contribution of p53 to numerous other aspects of disease and normal life is only now being appreciated. This burgeoning range of responses to p53 is reflected by an increasing variety of mechanisms through which p53 can function, although the ability to activate transcription remains key to p53's modus operandi. Control of p53's transcriptional activity is crucial for determining which p53 response is activated, a decision we must understand if we are to exploit efficiently the next generation of drugs that selectively activate or inhibit p53.
Overview
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
Verification
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?
In the citing paper
“Transient stress leads to induction of p53 which activates DNA repair and leads to quiescence (Vousden and Prives, 2009; Kasteri et al., 2018).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Vousden and Prives, 2009
In the citing paper
“Consequently, p53 target genes become activated and drive cellular responses of tumor cells, which include cell cycle arrest, apoptosis and senescence. 2”
From Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death (2013) · cites this paper as [2]
In the citing paper
“p53 is a key transcriptional regulator that controls multiple signals by activating genes with roles in cell cycle arrest, senescence, apoptosis, metabolism, differentiation, and survival (Vousden and Prives, 2009).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Vousden and Prives, 2009
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
RETRACTED: hnRNP K: An HDM2 Target and Transcriptional Coactivator of p53 in Response to DNA Damage
Moumen, A., Masterson, P., O'Connor, M. J., & Jackson, S. P. (2005) · Cell · doi:10.1016/j.cell.2005.09.032 · Cited by 350
RetractedIn 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
The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation
DeBerardinis, R. J., Lum, J. J., Hatzivassiliou, G., & Thompson, C. B. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2007.10.002 · Cited by 4,088
The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth
Christofk, H. R., Vander Heiden, M. G., Harris, M. H., Ramanathan, A., Gerszten, R. E., Wei, R., Fleming, M. D., Schreiber, S. L., & Cantley, L. C. (2008) · Nature · doi:10.1038/nature06734 · Cited by 2,820
A microRNA component of the p53 tumour suppressor network
He, L., He, X., Lim, L. P., de Stanchina, E., Xuan, Z., Liang, Y., Xue, W., Zender, L., Magnus, J., Ridzon, D., et al. (2007) · Nature · doi:10.1038/nature05939 · Cited by 2,692
Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
Vousden, K. H., & Lane, D. P. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2147 · Cited by 2,351
Self-citationTIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis
Bensaad, K., Tsuruta, A., Selak, M. A., Vidal, M. N. C., Nakano, K., Bartrons, R., Gottlieb, E., & Vousden, K. H. (2006) · Cell · doi:10.1016/j.cell.2006.05.036 · Cited by 2,019
Self-citationTransactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis
Chang, T.-C., Wentzel, E. A., Kent, O. A., Ramachandran, K., Mullendore, M., Lee, K. H., Feldmann, G., Yamakuchi, M., Ferlito, M., Lowenstein, C. J., et al. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.05.010 · Cited by 2,010
Transcriptional control of human p53-regulated genes
Riley, T., Sontag, E., Chen, P., & Levine, A. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2395 · Cited by 1,921
Flagged first, then by citations
1 of the 232 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Items 1,001–1,016 of 1,016
Insights into regulators of p53 acetylation
Nagasaka, M., Miyajima, C., Aoki, H., Aoyama, M., Morishita, D., Inoue, Y., & Hayashi, H. (2022) · Cells · doi:10.3390/cells11233825 · Cited by 45
Druggable Orthosteric and Allosteric Hot Spots to Target Protein-protein Interactions
Ma, B., & Nussinov, R. (2014) · Current Pharmaceutical Design · doi:10.2174/13816128113199990073 · Cited by 45
Dulic, V. (2013) · Methods in Molecular Biology · doi:10.1007/978-1-62703-239-1_2 · Cited by 42
Zhan, H., Xie, H., Zhou, Q., Liu, Y., & Huang, W. (2018) · ACS Synthetic Biology · doi:10.1021/acssynbio.8b00202 · Cited by 36
The emerging functions of the p53-miRNA network in stem cell biology
Lin, C.-P., Choi, Y. J., Hicks, G. G., & He, L. (2012) · Cell Cycle · doi:10.4161/cc.20207 · Cited by 38
Removing all obstacles: A critical role for p53 in promoting tissue renewal
Schoppy, D. W., Ruzankina, Y., & Brown, E. J. (2010) · Cell Cycle · doi:10.4161/cc.9.7.11194 · Cited by 32
“While the overall outcome of p53 activation on a given cell can be varied and context dependent, DNA damage- and oncogeneinduced stabilization of p53 can limit the proliferative lifespan of cells.(12,13) As such, broad engagement of p53 in a proliferative tissue could be expected to restrict regenerative capacity and…”
BackgroundLigand dependent restoration of human TLR3 signaling and death in p53 mutant cells
Menendez, D., Lowe, J. M., Snipe, J., & Resnick, M. A. (2016) · Oncotarget · doi:10.18632/oncotarget.11210 · Cited by 31
Conradt, L., Henrich, A., Wirth, M., Reichert, M., Lesina, M., Algül, H., Schmid, R. M., Krämer, O. H., Saur, D., & Schneider, G. (2013) · International Journal of Cancer · doi:10.1002/ijc.27916 · Cited by 30
Estimating the Distribution of Protein Post-Translational Modification States by Mass Spectrometry
Compton, P. D., Kelleher, N. L., & Gunawardena, J. (2018) · Journal of Proteome Research · doi:10.1021/acs.jproteome.8b00150 · Cited by 30
Chen, H., Luo, D., Zhang, L., Lin, X., Luo, Q., Yi, H., Wang, J., Yan, X., Li, B., Chen, Y., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.17398 · Cited by 29
DNA damage response in proliferating Müller glia in the mammalian retina
Nomura-Komoike, K., Saitoh, F., Komoike, Y., & Fujieda, H. (2016) · Investigative Opthalmology & Visual Science · doi:10.1167/iovs.15-18101 · Cited by 25
Phosphorylation of Daxx by ATM contributes to DNA damage-induced p53 activation.
Tang, J., Agrawal, T., Cheng, Q., Qu, L., Brewer, M. D., Chen, J., & Yang, X. (2013) · PLoS ONE · doi:10.1371/journal.pone.0055813 · Cited by 28
Taylor, S., Hu, R., Pacheco, E., Locher, K., Pyrah, I., Ominsky, M. S., & Boyce, R. W. (2018) · Bone Reports · doi:10.1016/j.bonr.2018.03.002 · Cited by 25
PDBminer to Find and Annotate Protein Structures for Computational Analysis
Degn, K., Beltrame, L., Tiberti, M., & Papaleo, E. (2023) · doi:10.1101/2023.05.06.539447 · Cited by 6
Liu, O.-G., Xiong, X.-Y., Li, C.-M., Zhou, X.-S., & Li, S.-S. (2018) · Medical Science Monitor · doi:10.12659/msm.905319 · Cited by 4
Simplify p53: just an activator
Engeland, K. (2015) · Oncotarget · doi:10.18632/oncotarget.3032 · Cited by 3
Metadata
- Authors
- Vousden, K. H., & Prives, C.
- Affiliations
- Cancer Research UK Scotland Institute (GB)
- Columbia University (US)
- Corresponding author
- Vousden, Karen H.
- Prives, Carol
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2009-05
- Volume
- 137
- Issue
- 3
- Pages
- 413-431
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2133959309
- Semantic Scholar
- 018e8ed8c8694d45cfd9ffaf967368345fe22af6
- Cited by
- 3,163
- References
- 232
- Citations by year
- 2026: 128 · 2025: 154 · 2024: 127 · 2023: 168 · 2022: 149 · 2021: 166 · 2020: 175 · 2019: 149 · 2018: 171 · 2017: 191 · 2016: 228 · 2015: 202 · 2014: 258 · 2013: 263 · 2012: 228
- FWCI
- 17.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1538 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- Funders
- Cancer Research UK
- National Cancer Institute (R01CA077742, CA77742)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53, tumor suppressor, transcriptional activation, p53 activators, p53 inhibitors, p53 regulation
- MeSH terms
- Animals, Cell Survival, Cell Transformation, Neoplastic, Gene Expression Regulation, Humans, Mutation, Stress, Physiological, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, Cell Proliferation, Mice
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
