The DOI matches its Crossref record; 88 of the 88 references it cites were found in a registry or an index.
Transcriptional Cross Talk between NF-κB and p53
Open accessAbstract
Many cellular stimuli result in the induction of both the tumor suppressor p53 and NF-kappaB. In contrast to activation of p53, which is associated with the induction of apoptosis, stimulation of NF-kappaB has been shown to promote resistance to programmed cell death. These observations suggest that a regulatory mechanism must exist to integrate these opposing outcomes and coordinate this critical cellular decision-making event. Here we show that both p53 and NF-kappaB inhibit each other's ability to stimulate gene expression and that this process is controlled by the relative levels of each transcription factor. Expression of either wild-type p53 or the RelA(p65) NF-kappaB subunit suppresses stimulation of transcription by the other factor from a reporter plasmid in vivo. Moreover, endogenous, tumor necrosis factor alpha-activated NF-kappaB will inhibit endogenous wild-type p53 transactivation. Following exposure to UV light, however, the converse is observed, with p53 downregulating NF-kappaB-mediated transcriptional activation. Both p53 and RelA(p65) interact with the transcriptional coactivator proteins p300 and CREB-binding protein (CBP), and we demonstrate that these results are consistent with competition for a limiting pool of p300/CBP complexes in vivo. These observations have many implications for regulation of the transcriptional decision-making mechanisms that govern cellular processes such as apoptosis. Furthermore, they suggest a previously unrealized mechanism through which dysregulated NF-kappaB can contribute to tumorigenesis and disease.
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“Since p53 inhibits RELA by competing for CBP binding (Webster and Perkins, 1999), p53 likely limits the IL1 arm of the SASP by reducing NF-κB activity.”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Webster and Perkins, 1999
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Cites
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Sorted by citations
Shared Principles in NF-κB Signaling
Hayden, M. S., & Ghosh, S. (2008) · Cell · doi:10.1016/j.cell.2008.01.020 · Cited by 4,954
The complexity of NF-κB signaling in inflammation and cancer
Hoesel, B., & Schmid, J. A. (2013) · Molecular Cancer · doi:10.1186/1476-4598-12-86 · Cited by 3,277
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Self-citation
Metadata
- Authors
- Webster, G. A., & Perkins, N. D.
- Affiliations
- University of Dundee (GB)
- ORCID
- Perkins, Neil D.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1999-05-01
- Volume
- 19
- Issue
- 5
- Pages
- 3485-3495
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC84141
- OpenAlex
- W2134542375
- Cited by
- 598
- References
- 87
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 12 · 2023: 13 · 2022: 19 · 2021: 30 · 2020: 17 · 2019: 16 · 2018: 16 · 2017: 12 · 2016: 20 · 2015: 23 · 2014: 14 · 2013: 20 · 2012: 15
- FWCI
- 13.41
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Molecular and Cellular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Royal Society
- Tenovus
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- NF-κB, p53, transcriptional crosstalk, RelA/p65, P300, CREB-binding protein, transcriptional coactivator, apoptosis, TNF-α, transcriptional repression, carcinogenesis
- MeSH terms
- Binding, Competitive, Cell Line, Gene Expression Regulation, Humans, Mutation, Repressor Proteins, Transcription, Genetic, Tumor Necrosis Factor-alpha, Ultraviolet Rays, Trans-Activators, Tumor Suppressor Protein p53, NF-kappa B, Apoptosis, Genes, Reporter, Transcription Factor RelA
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