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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p53 inhibits RELA by competing for CBP binding.
“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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- [29]Horvai A E, Xu L, Korzus E, Brard G, Kalafus D, Mullen T M, Rose D W, Rosenfeld M G, Glass C K. Nuclear integration of JAK/STAT and Ras/AP-1 signaling by CBP and p300. Proc Natl Acad Sci USA. 1997;94:1074–1079. doi: 10.1073/pnas.94.4.1074. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
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- 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
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 ›
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