The DOI matches its Crossref record; 39 of the 40 references it cites were found in a registry or an index.
p53 Suppresses the Activation of the Bcl-2 Promoter by the Brn-3a POU Family Transcription Factor
Open accessAbstract
The Brn-3a POU family transcription factor has been shown to strongly activate expression of the Bcl-2 proto-oncogene and thereby protect neuronal cells from programmed cell death (apoptosis). This activation of the Bcl-2 promoter by Brn-3a is strongly inhibited by the p53 anti-oncogene protein. This inhibitory effect of p53 on Brn-3a-mediated transactivation is observed with nonoverlapping gene fragments containing either the Bcl-2 p1 or p2 promoters but is not observed with other Brn-3a-activated promoters such as in the gene encoding alpha-internexin or with an isolated Brn-3a binding site from the Bcl-2 promoter linked to a heterologous promoter. In contrast, p53 mutants, which are incapable of binding to DNA, do not affect Brn-3a-mediated activation of the Bcl-2 p1 and p2 promoters. Moreover, Brn-3a and p53 have been shown to bind to adjacent sites in the p2 promoter and to directly interact with one another, both in vitro and in vivo, with this interaction being mediated by the POU domain of Brn-3a and the DNA binding domain of p53. The significance of these effects is discussed in terms of the antagonistic effects of Bcl-2 and p53 on the rate of apoptosis and the overexpression of Brn-3a in specific tumor cell types.
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“Additional BCL-2 family members reported as p53 targets include BCL2190, 191 and BID192—but these are not directly regulated by p53 according to meta-analysis data18 (Supplementary Table S2).”
From Census and evaluation of p53 target genes (2017) · cites this paper as [190]
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Sorted by citations
Transcriptional control of human p53-regulated genes
Riley, T., Sontag, E., Chen, P., & Levine, A. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2395 · Cited by 1,921
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Metadata
- Authors
- Budhram-Mahadeo, V., Morris, P. J., Smith, M. D., Midgley, C. A., Boxer, L. M., & Latchman, D. S.
- Affiliations
- University College London (GB)
- University of Dundee (GB)
- Stanford Medicine (US)
- Corresponding author
- Latchman, David S.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1999-05
- Volume
- 274
- Issue
- 21
- Pages
- 15237-15244
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2131045322
- Cited by
- 144
- References
- 40
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 4 · 2020: 4 · 2019: 3 · 2018: 6 · 2017: 5 · 2016: 2 · 2015: 2 · 2014: 6 · 2013: 10 · 2012: 2
- FWCI
- 3.55
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- p53, Brn3a, POU transcription factors, Bcl-2, Bcl-2 promoter, transcriptional repression, protein-protein interaction, POU domain, DNA-binding domain, apoptosis, neuronal survival, alpha-internexin
- MeSH terms
- Cells, Cultured, DNA-Binding Proteins, Promoter Regions, Genetic, Transcription Factors, Genes, p53, Genes, bcl-2, Transcription Factor Brn-3
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