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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.
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“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
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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
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