Repression of transcription mediated at a thyroid hormone response element by the v-erb-A oncogene product.
Research output: Contribution to journal › Journal article › Research › peer-review
Several recent observations, such as the identification of the cellular homologue of the v-erb-A oncogene as a thyroid-hormone receptor, have strongly implicated nuclear oncogenes in transcriptional control mechanisms. The v-erb-A oncogene blocks the differentiation of erythroid cells, and changes the growth requirements of fibroblasts and erythroblasts. Mutations in v-erb-A protein have led to the loss of its affinity for thyroid hormones but do not affect its DNA-binding ability, a property required for biological activity. We report here the identification of a novel thyroid-hormone response element (TRE) in the long terminal repeat of Moloney murine leukaemia virus that binds the c-erb-A-alpha protein. The v-erb-A protein abolishes the responsiveness of this TRE to thyroid hormone, although it has a lower affinity than the normal receptor for the TRE. The data indicate that overexpressed v-erb-A protein negatively interferes with normal transcriptional-control mechanisms, and that amino-acid substitutions have altered its DNA-binding properties.
Original language | English |
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Journal | Nature |
Volume | 340 |
Issue number | 6230 |
Pages (from-to) | 242-4 |
Number of pages | 2 |
ISSN | 0028-0836 |
DOIs | |
Publication status | Published - 1989 |
Bibliographical note
Keywords: Base Sequence; Gene Expression Regulation; Immunosorbent Techniques; Moloney murine leukemia virus; Oncogene Proteins v-erbA; Oncogenes; Plasmids; Promoter Regions (Genetics); Receptors, Thyroid Hormone; Repetitive Sequences, Nucleic Acid; Retroviridae Proteins; Sequence Homology, Nucleic Acid; Simplexvirus; Thyroid Hormones; Transcription, Genetic; Transfection; Triiodothyronine
ID: 5070200