The DOI matches its Crossref record; 43 of the 44 references it cites were found in a registry or an index.
p53 is required for radiation-induced apoptosis in mouse thymocytes
Abstract
The p53 tumour suppressor gene is the most widely mutated gene in human tumorigenesis. p53 encodes a transcriptional activator whose targets may include genes that regulate genomic stability, the cellular response to DNA damage, and cell-cycle progression. Introduction of wild-type p53 into cell lines that have lost endogenous p53 function can cause growth arrest or induce a process of cell death known as apoptosis. During normal development, self-reactive thymocytes undergo negative selection by apoptosis, which can also be induced in immature thymocytes by other stimuli, including exposure to glucocorticoids and ionizing radiation. Although normal negative selection involves signalling through the T-cell receptor, the induction of apoptosis by other stimuli is poorly understood. We have investigated the requirement for p53 during apoptosis in mouse thymocytes. We report here that immature thymocytes lacking p53 die normally when exposed to compounds that may mimic T-cell receptor engagement and to glucocorticoids but are resistant to the lethal effects of ionizing radiation. These results demonstrate that p53 is required for radiation-induced cell death in the thymus but is not necessary for all forms of apoptosis.
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“The checkpoints also actively stimulate the repair processes [1–9] and, in higher eukaryotes, trigger the apoptotic response, if damage cannot be dealt with successfully [10–12].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [10]
In the citing paper
“In both the pigmentation induction and DNA repair activation processes, POMC/α-MSH functions as the crucial downstream target of the “guardian of genome” protein p53 (47).”
From Melanocyte-stimulating hormone directly enhances UV-Induced DNA repair in keratinocytes by a xeroderma pigmentosum group A-dependent mechanism (2010) · cites this paper as [47]
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Metadata
- Authors
- Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T.
- Affiliations
- Massachusetts Institute of Technology (US)
- University of Massachusetts Amherst (US)
- Venue
- Nature
- Published
- 1993-04
- Volume
- 362
- Issue
- 6423
- Pages
- 847-849
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2078581194
- Cited by
- 2,864
- References
- 44
- Citations by year
- 2026: 8 · 2025: 15 · 2024: 28 · 2023: 18 · 2022: 9 · 2021: 24 · 2020: 19 · 2019: 23 · 2018: 31 · 2017: 28 · 2016: 34 · 2015: 24 · 2014: 30 · 2013: 37 · 2012: 40
- FWCI
- 123.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- 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 › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- p53, radiation-induced apoptosis, thymocytes, ionizing radiation, negative selection, T cell receptor signaling, glucocorticoids, T cell development, tumor suppressor, radioresistance (biology)
- MeSH terms
- Animals, Cells, Cultured, Dexamethasone, Gamma Rays, Mice, Inbred C57BL, Mutation, Thymus Gland, Genes, p53, Tumor Suppressor Protein p53, Apoptosis, Mice
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