Active transcription of the human FAS/CD95/TNFRSF6 gene involves the p53 family
Abstract
p63 and p73 express two main classes of isoforms: isoforms which contain the transactivation domain (TAp73 and TAp63) executing transcriptional activity and dominant-negative isoforms which are truncated at the NH2-terminus acting as operant inhibitors of TAp73, TAp63 and wild-type p53, and thus possessing oncogenic potential. Like wt p53, TAp63 and TAp73 isoforms transactivate target genes that activate apoptosis signaling pathways. In an attempt to understand how the CD95 gene is regulated by the p53 family, we investigated the contributions of a p53-responsive element (RE) within the first intron of the CD95 gene as well as three elements within the promoter. The intronic element conferred transcriptional activation by p53, TAp63 and TAp73 and cooperated with the p53-REs in the promoter of the CD95 gene. Cooperation between the p53-REs in the promoter and the intronic p53-binding site resulted in maximal transcriptional activation of the CD95 gene by the p53 family.
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TNF receptors include the p53-induced targets FAS and TNFRSF10A-D; these can be activated by external stimuli such as binding with FASL or TNF-α, thereby leading to caspase-dependent apoptosis.
“TNF receptors include the p53-induced targets FAS47, 48, 49 and TNFRSF10A–D;38, 39 these can be activated by external stimuli such as binding with FASL or TNF-α, thereby leading to caspase-dependent apoptosis.178”
From Census and evaluation of p53 target genes (2017) · cites this paper as [49]
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Self-citation
- Authors
- Schilling, T., Schleithoff, E. S., Kairat, A., Melino, G., Stremmel, W., Oren, M., Krammer, P. H., & Müller, M.
- Affiliations
- University Hospital Heidelberg (DE)
- Heidelberg University (DE)
- University of Leicester (GB)
- Weizmann Institute of Science (IL)
- German Cancer Research Center (DE)
- Corresponding author
- Müller, Martina
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2009-09
- Volume
- 387
- Issue
- 2
- Pages
- 399-404
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2004445242
- Cited by
- 43
- References
- 20
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 3 · 2021: 1 · 2019: 1 · 2018: 6 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 6 · 2013: 1 · 2012: 3
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Helmholtz Association
- 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 › Genomics and Chromatin Dynamics
- Keywords
- p53 family, p63, p73, TAp63, TAp73, transcriptional activation, p53 response elements, promoter elements, apoptosis signaling, dominant-negative isoform
- MeSH terms
- Tumor Protein p73, Base Sequence, Binding Sites, DNA-Binding Proteins, Humans, Introns, Molecular Sequence Data, Nuclear Proteins, Promoter Regions, Genetic, Transcription Factors, Transcription, Genetic, Transcriptional Activation, Trans-Activators, Tumor Suppressor Protein p53, fas Receptor, Tumor Suppressor Proteins, Cell Line, Tumor
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