v-erbA oncogene activation entails the loss of hormone-dependent regulator activity of c-erbA

Cell. 1990 Jun 15;61(6):1035-49. doi: 10.1016/0092-8674(90)90068-p.


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.

MeSH terms

  • Alpharetrovirus / genetics*
  • Amino Acid Sequence
  • Animals
  • Antigens, Surface / analysis
  • Avian Leukosis Virus / genetics*
  • Cell Transformation, Neoplastic
  • Cells, Cultured
  • Chick Embryo
  • Clone Cells
  • Erythroblasts / enzymology
  • Erythrocytes / enzymology
  • Gene Expression Regulation* / drug effects
  • Genetic Vectors
  • Hemoglobins / biosynthesis
  • Molecular Sequence Data
  • Oncogene Proteins v-erbA
  • Oncogenes*
  • Protein Conformation
  • Protein-Tyrosine Kinases / genetics
  • Receptors, Thyroid Hormone / physiology*
  • Recombinant Fusion Proteins / biosynthesis
  • Retroviridae Proteins, Oncogenic / biosynthesis
  • Retroviridae Proteins, Oncogenic / genetics*
  • Retroviridae Proteins, Oncogenic / metabolism
  • Suppression, Genetic
  • Transcription, Genetic / drug effects*
  • Triiodothyronine / pharmacology*


  • Antigens, Surface
  • Hemoglobins
  • Oncogene Proteins v-erbA
  • Receptors, Thyroid Hormone
  • Recombinant Fusion Proteins
  • Retroviridae Proteins, Oncogenic
  • Triiodothyronine
  • Protein-Tyrosine Kinases