TEL Is a Sequence-specific Transcriptional Repressor
Open accessAbstract
TEL is a gene frequently involved in specific chromosomal translocations in human leukemia and sarcoma that encodes a member of the ETS family of transcriptional regulators. TEL is unusual among other ETS proteins by its ability to self-associate in vivo, a property that is essential to the oncogenic activation of TEL-derived fusion proteins. We show here that TEL is a sequence-specific transcriptional repressor of ETS-binding site-driven transcription of model and natural promoters. Deletion of the oligomerization domain of TEL or its substitution by the homologous region of monomeric ETS1 impaired the ability of TEL to repress. In contrast, substitution of the oligomerization domain of TEL by unrelated oligomerization domains resulted in an active repressor, showing that the ability of TEL to repress depends on its ability to self-associate. The study of the properties of TEL fusions to the heterologous DNA binding domain of Gal4 identified two autonomous repression domains in TEL, distinct from its oligomerization domain, that are essential to the ability of TEL to repress ETS-binding site-containing promoters. These results have implications for the normal function of TEL, its relation to other ETS proteins, and its role in leukemogenesis.
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TEL represses transcription through the Ets site, and repression may be attributed to recruitment of mSin3A, corepressor N-CoR, and histone deacetylase HDAC3.
“TEL represses transcription through the Ets site, and repression may be attributed to the recruitment of mSin3A, corepressor N-CoR, and histone deacetylase HDAC3 (7, 14, 29, 33, 55).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [29]
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- Authors
- Lopez, R. G., Carron, C., Oury, C., Gardellin, P., Bernard, O., & Ghysdael, J.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Inserm (FR)
- Corresponding author
- Ghysdael, Jacques
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1999-10
- Volume
- 274
- Issue
- 42
- Pages
- 30132-30138
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2083314849
- Cited by
- 174
- References
- 43
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 8 · 2016: 6 · 2015: 5 · 2014: 2 · 2013: 5 · 2012: 3
- FWCI
- 3.99
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ORBi (University of Liège) (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- TEL, ETS transcription factors, transcriptional repression, Ets binding site, protein self-association, oligomerization domain, leukemia, sarcoma, chromosomal translocation, oncogene activation, GAL4 DNA-binding domain
- MeSH terms
- ETS Translocation Variant 6 Protein, Animals, Base Sequence, Binding Sites, DNA-Binding Proteins, HeLa Cells, Humans, Promoter Regions, Genetic, Proto-Oncogene Proteins, Repressor Proteins, Transcription Factors, Transcription, Genetic, Trans-Activators, DNA Primers, Proto-Oncogene Proteins c-ets, Proto-Oncogene Protein c-ets-1, Mice, Proto-Oncogene Protein c-fli-1
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