Cited by 131Cancer-related Molecular PathwaysCell death mechanisms and regulationHeat shock proteins research

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Human and Mouse Fas (APO-1/CD95) Death Receptor Genes Each Contain a p53-responsive Element That Is Activated by p53 Mutants Unable to Induce Apoptosis

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Munsch, Dany, Watanabe-Fukunaga, Rie, Bourdon, Jean-Christophe, Nagata, Shigekasu, May, Evelyne, Yonish-Rouach, Elisheva, Reisdorf, Philippe·2000·Journal of Biological Chemistry

DOI 10.1074/jbc.275.6.3867

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Abstract

p53 is a tumor suppressor protein that induces apoptosis at least in part through its ability to act as a sequence-specific transactivator. This work reports that intron 1 of the mouse Fas death receptor gene contains a p53-responsive element (p53RE) that matches the p53 consensus sequence and that is located between nucleotides +1704 and +1723 from the transcription initiation site. This element is specifically bound by p53 and functions as a p53-dependent enhancer in mammalian or in yeast reporter gene assays. Contrary to bax, another known pro-apoptotic p53-target gene, both mouse and human FAS p53REs are still activated by the discriminatory p53 mutants Pro-175 and Ala-143, a class of mutants unable to induce apoptosis. We propose that p53-dependent up-regulation of Fas does not induce apoptosis per se but sensitizes the cell to other pro-apoptotic signal(s). The functional conservation of p53-dependent Fas up-regulation argues strongly in favor of its biological importance and suggests that murine models may be used to study further the in vivo role of Fas in the p53 response.

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Authors: Munsch, D., Watanabe-Fukunaga, R., Bourdon, J.-C., Nagata, S., May, E., Yonish-Rouach, E., & Reisdorf, P.
Affiliations: Centre National de la Recherche Scientifique (FR)
The University of Osaka (JP)
Corresponding author: Reisdorf, Philippe
ORCID: Bourdon, Jean-Christophe
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 2000-02
Volume: 275
Issue: 6
Pages: 3867-3872
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.275.6.3867
OpenAlex: W2022923458
Cited by: 131
References: 53
Citations by year: 2025: 1 · 2024: 5 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 14 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 1 · 2015: 3 · 2014: 2 · 2012: 3
FWCI: 6.92
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 7554 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Discovery Research Portal (University of Dundee) (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 › Heat shock proteins research
Keywords: Fas, p53 response elements, p53, intron 1, mutant p53, apoptosis sensitization, Bax, tumor suppressor
MeSH terms: Animals, Cell Line, Humans, Mutation, Promoter Regions, Genetic, Protein Binding, Transfection, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, Genes, Reporter, fas Receptor, Mice

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Human and Mouse Fas (APO-1/CD95) Death Receptor Genes Each Contain a p53-responsive Element That Is Activated by p53 Mutants Unable to Induce Apoptosis

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