Cited by 568Cancer-related Molecular PathwaysGenomics and Chromatin DynamicsChromatin Remodeling and Cancer

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The expanding universe of p53 targets

Menendez, Daniel, Inga, Alberto, Resnick, Michael A.·2009·Nature Reviews Cancer

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Abstract

The p53 tumour suppressor is modified through mutation or changes in expression in most cancers, leading to the altered regulation of hundreds of genes that are directly influenced by this sequence-specific transcription factor. Central to the p53 master regulatory network are the target response element (RE) sequences. The extent of p53 transactivation and transcriptional repression is influenced by many factors, including p53 levels, cofactors and the specific RE sequences, all of which contribute to the role that p53 has in the aetiology of cancer. This Review describes the identification and functionality of REs and highlights the inclusion of non-canonical REs that expand the universe of genes and regulation mechanisms in the p53 tumour suppressor network.

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MED1/TRAP220 Exists Predominantly in a TRAP/ Mediator Subpopulation Enriched in RNA Polymerase II and Is Required for ER-Mediated Transcription
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p53 Suppresses the Activation of the Bcl-2 Promoter by the Brn-3a POU Family Transcription Factor
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p73 or p53 Directly Regulates Human p53 Transcription to Maintain Cell Cycle Checkpoints
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Noncanonical DNA Motifs as Transactivation Targets by Wild Type and Mutant p53
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A new p38 MAP kinase‐regulated transcriptional coactivator that stimulates p53‐dependent apoptosis
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p63 consensus DNA-binding site: identification, analysis and application into a p63MH algorithm
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Repression of CDK1 and Other Genes with CDE and CHR Promoter Elements during DNA Damage-Induced G 2 /M Arrest in Human Cells
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A SNP in the flt-1 promoter integrates the VEGF system into the p53 transcriptional network
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The biological impact of the human master regulator p53 can be altered by mutations that change the spectrum and expression of its target genes
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The Human Caspase-8 Promoter Sustains Basal Activity through SP1 and ETS-like Transcription Factors and Can Be Up-regulated by a p53-dependent Mechanism
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Estrogen receptor protects p53 from deactivation by human double minute-2.
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p53 Target Gene SMAR1 Is Dysregulated in Breast Cancer: Its Role in Cancer Cell Migration and Invasion
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p53 promoter selection: Choosing between life and death
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Crippling p53 activities via knock-in mutations in mouse models
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LIM and SH3 protein 1 (Lasp1) is a novel p53 transcriptional target involved in hepatocellular carcinoma
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CA/TG sequence at the 5' end of oligo(A)-tracts strongly modulates DNA curvature.
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Chromatin Immunoprecipitation-Based Screen To Identify Functional Genomic Binding Sites for Sequence-Specific Transactivators
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The transcription factor PAX4 acts as a survival gene in INS-1E insulinoma cells
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Estrogen receptor acting in cis enhances WT and mutant p53 transactivation at canonical and noncanonical p53 target sequences
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Negative Regulation of Chk2 Expression by p53 Is Dependent on the CCAAT-binding Transcription Factor NF-Y
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See all 568

Authors: Menendez, D., Inga, A., & Resnick, M. A.
Affiliations: National Institutes of Health (US)
Corresponding author: Resnick, Michael A.
ORCID: Inga, Alberto
Resnick, Michael A.
Venue: Nature Reviews Cancer
Publisher: Springer Science and Business Media LLC
Published: 2009-10
Volume: 9
Issue: 10
Pages: 724-737
ISSN: 1474-175X (ISSN-L)
1474-1768
DOI: 10.1038/nrc2730
OpenAlex: W2094375196
Cited by: 568
References: 208
Citations by year: 2026: 11 · 2025: 8 · 2024: 11 · 2023: 17 · 2022: 28 · 2021: 18 · 2020: 23 · 2019: 28 · 2018: 31 · 2017: 42 · 2016: 44 · 2015: 44 · 2014: 54 · 2013: 59 · 2012: 56
FWCI: 4.10
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Cancer (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute of Environmental Health Sciences (Z01ES065079)
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 › Chromatin Remodeling and Cancer
Keywords: p53, transcriptional regulation, tumour suppressor, p53 target genes, p53 transactivation, transcriptional repression, cancer etiology
MeSH terms: Humans, Mutation, Neoplasms, Gene Expression, Genes, p53, Tumor Suppressor Protein p53, Response Elements

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