The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Differential Transactivation by the p53 Transcription Factor Is Highly Dependent on p53 Level and Promoter Target Sequence
Open accessAbstract
Little is known about the mechanisms that regulate differential transactivation by p53. We developed a system in the yeast Saccharomyces cerevisiae that addresses p53 transactivation capacity from 26 different p53 response elements (REs) under conditions where all other factors, such as chromatin, are kept constant. The system relies on a tightly regulated promoter (rheostatable) that can provide for a broad range of p53 expression. The p53 transactivation capacity toward each 20- to 22-bp-long RE could be ranked by using a simple phenotypic assay. Surprisingly, there was as much as a 1,000-fold difference in transactivation. There was no correlation between the functional rank and statistical predictions of binding energy of the REs. Instead we found that the central sequence element in an RE greatly affects p53 transactivation capacity, possibly because of DNA structural properties. Our results suggest that intrinsic DNA binding affinity and p53 protein levels are important contributors to p53-induced differential transactivation. These results are also relevant to understanding the regulation by other families of transcription factors that recognize several sequence-related response elements and/or have tightly regulated expression. We found that p53 had weak activity towards half the apoptotic REs. In addition, p53 alleles associated with familial breast cancer, previously classified as wild type, showed subtle differences in transactivation capacity towards several REs.
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Cites
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BackgroundMdm2 promotes the rapid degradation of p53
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“, positions 3 and 4, as predicted by the crystal structure (16).”
BackgroundInfluentialNoxa, a BH3-Only Member of the Bcl-2 Family and Candidate Mediator of p53-Induced Apoptosis
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Definition of a consensus binding site for p53
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Transcriptional activation by recruitment
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“variation in nucleotide sequence, reflected by a loose consensus within a family (51, 60).”
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ASPP Proteins Specifically Stimulate the Apoptotic Function of p53
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Cited by
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
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
DNA damage and the balance between survival and death in cancer biology
Roos, W. P., Thomas, A. D., & Kaina, B. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2015.2 · Cited by 1,189
The multiple mechanisms that regulate p53 activity and cell fate
Hafner, A., Bulyk, M. L., Jambhekar, A., & Lahav, G. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0110-x · Cited by 1,129
TP53 mutations in human cancers: Functional selection and impact on cancer prognosis and outcomes
Petitjean, A., Achatz, M. I. W., Borresen-Dale, A. L., Hainaut, P., & Olivier, M. (2007) · Oncogene · doi:10.1038/sj.onc.1210302 · Cited by 884
Metadata
- Authors
- Inga, A., Storici, F., Darden, T. A., & Resnick, M. A.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2002-12-01
- Volume
- 22
- Issue
- 24
- Pages
- 8612-8625
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2112287022
- Cited by
- 199
- References
- 13
- FWCI
- 3.98
- Type
- journal article
- Language
- en
- Open access
- green
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- Inga, A., Storici, F., Darden, T. A., & Resnick, M. A. (2002). Differential Transactivation by the p53 Transcription Factor Is Highly Dependent on p53 Level and Promoter Target Sequence. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.22.24.8612-8625.2002
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