v-erbA oncogene activation entails the loss of hormone-dependent regulator activity of c-erbA.
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v-erbA oncogene activation entails the loss of hormone-dependent regulator activity of c-erbA. / Zenke, M; Muñoz, A; Sap, J; Vennström, B; Beug, H.
In: Cell, Vol. 61, No. 6, 1990, p. 1035-49.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - v-erbA oncogene activation entails the loss of hormone-dependent regulator activity of c-erbA.
AU - Zenke, M
AU - Muñoz, A
AU - Sap, J
AU - Vennström, B
AU - Beug, H
N1 - Keywords: Alpharetrovirus; Amino Acid Sequence; Animals; Antigens, Surface; Avian leukosis virus; Cell Transformation, Neoplastic; Cells, Cultured; Chick Embryo; Clone Cells; Erythroblasts; Erythrocytes; Gene Expression Regulation; Genetic Vectors; Hemoglobins; Molecular Sequence Data; Oncogene Proteins v-erbA; Oncogenes; Protein Conformation; Protein-Tyrosine Kinases; Receptors, Thyroid Hormone; Recombinant Fusion Proteins; Retroviridae Proteins, Oncogenic; Suppression, Genetic; Transcription, Genetic; Triiodothyronine
PY - 1990
Y1 - 1990
N2 - The v-erbA oncogene, one of the two oncogenes of the avian erythroblastosis virus, efficiently blocks erythroid differentiation and suppresses erythrocyte-specific gene transcription. Here we show that the overexpressed thyroid hormone receptor c-erbA effectively modulates erythroid differentiation and erythrocyte-specific gene expression in a T3-dependent fashion, when introduced into erythroid cells via a retrovirus. In contrast, the endogenous thyroid hormone receptor does not detectably affect erythroid differentiation. The analysis of a series of chimeric v-/c-erbA proteins suggests that the v-erbA oncoprotein has lost one type of thyroid hormone receptor function (regulating erythrocyte gene transcription in response to T3), but constitutively displays another function: it represses transcription in the absence of T3. The region responsible for the loss of hormone-dependent regulator activity of v-erbA has been mapped to the very C-terminus of c-erbA, encompassing a cluster of highly conserved amino acid residues with the potential to form an amphipathic alpha-helix.
AB - The v-erbA oncogene, one of the two oncogenes of the avian erythroblastosis virus, efficiently blocks erythroid differentiation and suppresses erythrocyte-specific gene transcription. Here we show that the overexpressed thyroid hormone receptor c-erbA effectively modulates erythroid differentiation and erythrocyte-specific gene expression in a T3-dependent fashion, when introduced into erythroid cells via a retrovirus. In contrast, the endogenous thyroid hormone receptor does not detectably affect erythroid differentiation. The analysis of a series of chimeric v-/c-erbA proteins suggests that the v-erbA oncoprotein has lost one type of thyroid hormone receptor function (regulating erythrocyte gene transcription in response to T3), but constitutively displays another function: it represses transcription in the absence of T3. The region responsible for the loss of hormone-dependent regulator activity of v-erbA has been mapped to the very C-terminus of c-erbA, encompassing a cluster of highly conserved amino acid residues with the potential to form an amphipathic alpha-helix.
M3 - Journal article
C2 - 1972036
VL - 61
SP - 1035
EP - 1049
JO - Cell
JF - Cell
SN - 0092-8674
IS - 6
ER -
ID: 5070162