Abstract |
The mouse mammary tumor virus long terminal repeat (LTR) is a potent transcriptional enhancer. We identified several putative binding sites for the TEF-1 family of transcription factors (TEF-1, RTEF-1, DTEF-1, and ETF) in the proximal negative regulatory element of the LTR. Gel mobility shift assays revealed strong TEF-1 factor binding to one site using nuclear extracts from CV-1 cells and from the human breast cancer cell line MCF-7. Mutation of this site increased basal activity of the LTR. In transient transfection assays, TEF-1 squelched the basal LTR activity and completely abrogated the response to the glucocorticoid dexamethasone. RTEF-1 and DTEF-1 had little effect on the basal activity, whereas ETF activated the LTR. These TEF-1 factors also interfered with the response to dexamethasone. Taken together, our results reveal an important new role for TEF-1 factors in regulating MMTV LTR activity and suggest that TEF-1 factors might participate in mammary tumorigenesis.
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Authors | Tomoji Maeda, Mamiko Maeda, Alexandre F R Stewart |
Journal | Biochemical and biophysical research communications
(Biochem Biophys Res Commun)
Vol. 296
Issue 5
Pg. 1279-85
(Sep 06 2002)
ISSN: 0006-291X [Print] United States |
PMID | 12207913
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- DNA-Binding Proteins
- DTEF-1 protein, Gallus gallus
- Glucocorticoids
- Muscle Proteins
- Nuclear Proteins
- TEA Domain Transcription Factors
- TEAD1 protein, human
- TEAD4 protein, human
- Tead3 protein, mouse
- Trans-Activators
- Transcription Factors
- Dexamethasone
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Topics |
- Base Sequence
- Binding Sites
- Cell Line
- DNA-Binding Proteins
(physiology)
- Dexamethasone
(antagonists & inhibitors)
- Gene Expression Regulation, Viral
- Glucocorticoids
(antagonists & inhibitors)
- Humans
- Mammary Tumor Virus, Mouse
(genetics)
- Molecular Sequence Data
- Muscle Proteins
(physiology)
- Nuclear Proteins
- Promoter Regions, Genetic
- TEA Domain Transcription Factors
- Terminal Repeat Sequences
- Trans-Activators
(physiology)
- Transcription Factors
(physiology)
- Transcription, Genetic
- Tumor Cells, Cultured
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