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Cell Type- and Promoter-specific Roles of Ser18 Phosphorylation in Regulating p53 Responses
Open accessAbstract
Phosphorylation of mouse p53 at Ser18 occurs after DNA damage. To determine the physiological roles of this phosphorylation event in p53-dependent DNA damage responses, a Ser18 to Ala missense mutation was introduced into the germline of mice. Thymocytes and fibroblasts from the knock-in mice show reduced transactivation of many p53 target genes following DNA damage. p53 protein stabilization and DNA binding are similar in knock-in and wild type mice, but C-terminal acetylation was defective, consistent with a role for Ser18 in the recruitment of transcriptional co-activators. The apoptotic response of knock-in thymocytes to ionizing radiation is intermediate between that of wild type and p53 null thymocytes. Despite impaired transcriptional and apoptotic responses, the knock-in mice are not prone to spontaneous tumorigenesis. This indicates that neither phosphorylation of p53 on Ser18 by ATM nor a full transcriptional response is essential to prevent spontaneous tumor formation in mice.
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“However, mutations of phosphorylation sites for these kinases on p53 and MDM2 or siRNA knockdown of Chk1 and Chk2 kinases lead to partial or no phenotypes (Wu et al, 2002;Ahn et al, 2003;Chao et al, 2003;Sluss et al, 2004), suggesting that additional targets and mechanisms may also contribute to activation of p53 after DNA damage.”
From ATM and Chk2-dependent phosphorylation of MDMX contribute to p53 activation after DNA damage (2005) · cites this paper as Chao et al, 2003
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Metadata
- Authors
- Chao, C., Hergenhahn, M., Kaeser, M. D., Wu, Z., Saito, S., Iggo, R., Hollstein, M., Appella, E., & Xu, Y.
- Affiliations
- University of California San Diego (US)
- German Cancer Research Center (DE)
- National Institutes of Health (US)
- Corresponding author
- Xu, Yang
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-10
- Volume
- 278
- Issue
- 42
- Pages
- 41028-41033
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2029715841
- Cited by
- 141
- References
- 31
- Citations by year
- 2025: 1 · 2023: 1 · 2021: 1 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 6 · 2013: 9 · 2012: 11
- FWCI
- 5.26
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- National Cancer Institute (R01CA094254, CA94254)
- 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 › Cell death mechanisms and regulation
- Keywords
- p53, DNA damage response, ATM kinase, transcriptional coactivator, thymocytes, fibroblasts, spontaneous tumor development
- MeSH terms
- Animals, Cell Cycle, Chromatin, DNA Damage, DNA-Binding Proteins, Dose-Response Relationship, Radiation, Fibroblasts, Mice, Transgenic, Phosphorylation, Precipitin Tests, Promoter Regions, Genetic, RNA, Messenger, Serine, Thymus Gland, Time Factors, Transcription, Genetic, Ultraviolet Rays, Blotting, Western, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, Protein Serine-Threonine Kinases, Protein Structure, Tertiary, Cell Cycle Proteins, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Tumor Suppressor Proteins, Mice, Ataxia Telangiectasia Mutated Proteins
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