Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1990-7-18
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1035-49
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:1972036-Alpharetrovirus, pubmed-meshheading:1972036-Amino Acid Sequence, pubmed-meshheading:1972036-Animals, pubmed-meshheading:1972036-Antigens, Surface, pubmed-meshheading:1972036-Avian leukosis virus, pubmed-meshheading:1972036-Cell Transformation, Neoplastic, pubmed-meshheading:1972036-Cells, Cultured, pubmed-meshheading:1972036-Chick Embryo, pubmed-meshheading:1972036-Clone Cells, pubmed-meshheading:1972036-Erythroblasts, pubmed-meshheading:1972036-Erythrocytes, pubmed-meshheading:1972036-Gene Expression Regulation, pubmed-meshheading:1972036-Genetic Vectors, pubmed-meshheading:1972036-Hemoglobins, pubmed-meshheading:1972036-Molecular Sequence Data, pubmed-meshheading:1972036-Oncogene Proteins v-erbA, pubmed-meshheading:1972036-Oncogenes, pubmed-meshheading:1972036-Protein Conformation, pubmed-meshheading:1972036-Protein-Tyrosine Kinases, pubmed-meshheading:1972036-Receptors, Thyroid Hormone, pubmed-meshheading:1972036-Recombinant Fusion Proteins, pubmed-meshheading:1972036-Retroviridae Proteins, Oncogenic, pubmed-meshheading:1972036-Suppression, Genetic, pubmed-meshheading:1972036-Transcription, Genetic, pubmed-meshheading:1972036-Triiodothyronine
pubmed:year
1990
pubmed:articleTitle
v-erbA oncogene activation entails the loss of hormone-dependent regulator activity of c-erbA.
pubmed:affiliation
Institute of Molecular Pathology, Vienna, Austria.
pubmed:publicationType
Journal Article