Mutation of Mouse p53 Ser23 and the Response to DNA Damage
Open accessAbstract
Recent studies have suggested that phosphorylation of human p53 at Ser20 is important for stabilizing p53 in response to DNA damage through disruption of the interaction between MDM2 and p53. To examine the requirement for this DNA damage-induced phosphorylation event in a more physiological setting, we introduced a missense mutation into the endogenous p53 gene of mouse embryonic stem (ES) cells that changes serine 23 (S23), the murine equivalent of human serine 20, to alanine (A). Murine embryonic fibroblasts harboring the p53(S23A) mutation accumulate p53 as well as p21 and Mdm2 proteins to normal levels after DNA damage. Furthermore, ES cells and thymocytes harboring the p53(S23A) mutation also accumulate p53 protein to wild-type levels and undergo p53-dependent apoptosis similarly to wild-type cells after DNA damage. Therefore, phosphorylation of murine p53 at Ser23 is not required for p53 responses to DNA damage induced by UV and ionizing radiation treatment.
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Mouse studies show that blocking p53 phosphorylation at corresponding serine residues only caused modest defects in p53-mediated apoptosis and tumor suppression function.
“Moreover, mouse studies show that blocking p53 phosphorylation at corresponding serine residues only caused modest defects in p53-mediated apoptosis and tumor suppression function [70–73].”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [73]
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References 43 · Cited by 103
- Authors
- Wu, Z., Earle, J., Saito, S., Anderson, C. W., Appella, E., & Xu, Y.
- Affiliations
- University of California San Diego (US)
- Laboratory of Cell Biology, National Cancer Institute, National Institute of Health, Bethesda, Maryland 20892
- Brookhaven National Laboratory (US)
- National Institutes of Health (US)
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2002-04-01
- Volume
- 22
- Issue
- 8
- Pages
- 2441-2449
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC133708
- OpenAlex
- W2150611871
- Cited by
- 103
- References
- 43
- Citations by year
- 2025: 1 · 2023: 1 · 2020: 3 · 2019: 4 · 2018: 1 · 2016: 3 · 2015: 3 · 2014: 5 · 2013: 4 · 2012: 4
- FWCI
- 5.77
- 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)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Keywords
- p53, DNA damage response, MDM2, p53 stabilization, p21, apoptosis, mouse embryonic stem cells, thymocytes, UV irradiation, ionizing radiation
- MeSH terms
- Animals, Cell Line, DNA Damage, Humans, Nuclear Proteins, Phosphorylation, Proto-Oncogene Proteins, T-Lymphocytes, Ultraviolet Rays, Genes, p53, Tumor Suppressor Protein p53, Mutagenesis, Site-Directed, Apoptosis, Amino Acid Substitution, Mutation, Missense, Mice, Proto-Oncogene Proteins c-mdm2
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