The DOI matches its Crossref record; 201 of the 201 references it cites were found in a registry or an index.
Transcriptional control of human p53-regulated genes
Abstract
The p53 protein regulates the transcription of many different genes in response to a wide variety of stress signals. Following DNA damage, p53 regulates key processes, including DNA repair, cell-cycle arrest, senescence and apoptosis, in order to suppress cancer. This Analysis article provides an overview of the current knowledge of p53-regulated genes in these pathways and others, and the mechanisms of their regulation. In addition, we present the most comprehensive list so far of human p53-regulated genes and their experimentally validated, functional binding sites that confer p53 regulation.
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In the citing paper
“The tumor suppressor p53 functions primarily as a transcription factor.”
From Census and evaluation of p53 target genes (2017) · cites this paper as [5]
In the citing paper
“The prevailing function of the p53 tumor suppressor is the transcriptional control of target genes that regulate numerous cellular processes, including cell cycle and apoptosis.5, 6”
From Census and evaluation of p53 target genes (2017) · cites this paper as [5]
In the citing paper
“p53 is an crucial tumor suppressor that is mutated in more than 50% of human cancers”
From USP10 Regulates p53 Localization and Stability by Deubiquitinating p53 (2010) · cites this paper as Riley et al., 2008
Citations
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“These include several types of DNA damage: telomere shortening, hypoxia, mitotic spindle damage, heat or cold shock, unfolded proteins, improper ribosomal biogenesis, nutritional deprivation in a transformed cell, and even the activation of some oncogenes by mutatio”
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BackgroundHistone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer
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Wild-type p53 induces apoptosis of myeloid leukaemic cells that is inhibited by interleukin-6
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Cited by
Sorted by citations
The DNA-damage response in human biology and disease
Jackson, S. P., & Bartek, J. (2009) · Nature · doi:10.1038/nature08467 · Cited by 6,092
The DNA Damage Response: Making It Safe to Play with Knives
Ciccia, A., & Elledge, S. J. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.019 · Cited by 4,368
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
TP53 mutations in human cancers: origins, consequences, and clinical use.
Olivier, M., Hollstein, M., & Hainaut, P. (2010) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001008 · Cited by 2,199
Self-consumption: the interplay of autophagy and apoptosis
Mariño, G., Niso-Santano, M., Baehrecke, E. H., & Kroemer, G. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3735 · Cited by 2,172
Metadata
- Authors
- Riley, T., Sontag, E., Chen, P., & Levine, A.
- Affiliations
- Institute for Advanced Study (US)
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Riley, Todd
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2008-05
- Volume
- 9
- Issue
- 5
- Pages
- 402-412
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W1964719993
- Cited by
- 1,921
- References
- 201
- Citations by year
- 2026: 36 · 2025: 45 · 2024: 56 · 2023: 73 · 2022: 85 · 2021: 97 · 2020: 79 · 2019: 92 · 2018: 110 · 2017: 134 · 2016: 131 · 2015: 115 · 2014: 154 · 2013: 143 · 2012: 153
- FWCI
- 12.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- p53, transcriptional regulation, p53 target genes, DNA damage response, DNA repair, cell cycle arrest, senescence, apoptosis, tumor suppression, transcription factor binding sites, stress signaling
- MeSH terms
- Base Sequence, Binding Sites, Cell Transformation, Neoplastic, DNA Damage, Gene Expression Regulation, Humans, Markov Chains, Molecular Sequence Data, Regulatory Sequences, Nucleic Acid, Transcription, Genetic, Signal Transduction, Genes, p53, Tumor Suppressor Protein p53, Response Elements, Regulatory Elements, Transcriptional
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