v-erbA specifically suppresses transcription of the avian erythrocyte anion transporter (Band 3) gene

  title={v-erbA specifically suppresses transcription of the avian erythrocyte anion transporter (Band 3) gene},
  author={Martin Zenke and Patricia Kahn and Christine Disela and Björn Vennström and Achim Leutz and Kathleen Keegan and Michael J Hayman and Hyeong Choi and Nelson Yew and James Douglas Engel and Hartmut Beug},
Phosphorylation of the v-erbA protein is required for its function as an oncogene.
The hypothesis that phosphorylation of the gag/v-erbA protein is important for transcriptional repression of at least some of its target genes in erythroid cells is supported.
Induction of differentiation of avian erythroblastosis virus-transformed erythroblasts by the protein kinase inhibitor H7: analysis of the transcription factor EF1.
  • R. Nicolas, G. Partington, G. Goodwin
  • Biology
    Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
  • 1991
It is concluded thatv-erbA and v-erbB do not repress differentiation by limiting the levels of EF1, and, although there may be a small change when the cells are shifted to 42 degrees C, incubation of the cells with H7 does not result in a further elevation commensurate with the high levels of globin transcripts.
Repression of transcription mediated at a thyroid hormone response element by the v-erb-A oncogene product
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.
Genetic dissection of functional domains within the avian erythroblastosis virus v-erbA oncogene
The results suggest that the mechanism of action of the v-erbA protein in establishing the neoplastic phenotype is closely related to its ability to interact with DNA, presumably thereby altering expression of host target genes by either mimicking or interfering with theaction of the normal c-erbB gene product.
Large-scale analysis by SAGE reveals new mechanisms of v-erbA oncogene action
15 of the new v-ErbA target genes were identified and demonstrated by real time PCR that in majority their expression was activated neither by T3, nor RA, nor during differentiation, which was unexpected based upon the previously known role of v- ErbA.
Transcriptional regulation by v-ErbA, the oncogenic counterpart of thyroid hormone receptor (TR)
The data suggest that v-ErbA prevents CA II activation by ‘neutralizing’ in cis the activity of erythroid transcription factors.
v-erbA overexpression is required to extinguish c-erbA function in erythroid cell differentiation and regulation of the erbA target gene CAII.
It is shown that v-erbA and c-erb a bind directly to sequences within the promoter of the erythrocyte-specific carbonic anhydrase II (CAII), a gene whose transcription is efficiently suppressed by v- DerbA.
Ontogeny of the v-erbA oncoprotein from the thyroid hormone receptor: an alteration in the DNA binding domain plays a role crucial for v-erbA function
Back mutation of the viral coding sequence to resemble c-erbA at this site severely impairs erythroid transformation and produces subtle changes in DNA binding by the encoded protein, suggesting that differences in DNAbinding by the viral and cellular proteins may be involved in the activation of v-erbC as an oncogene.


Control of erythroid differentiation: asynchronous expression of the anion transporter and the peripheral components of the membrane skeleton in AEV- and S13-transformed cells
Results suggest that during erythropoiesis, expression of the peripheral components of the membrane skeleton is initiated earlier than that of the anion transporter, and point a key role for the anions transporter in conferring long-term stability to the assembled erythroid membrane skeleton during terminal differentiation.
The chicken c-erbA proto-oncogene is preferentially expressed in erythrocytic cells during late stages of differentiation.
Results suggest that the c-erbA genes play some role in erythrocyte differentiation, and in situ hybridization on fractionated embryonic blood cells showed that c-urbA transcripts were predominantly found in ERYthroblasts, particularly during the final step of differentiation.
Enhanced transcription of c-myc in bursal lymphoma cells requires continuous protein synthesis.
The results suggest that a labile, cell type-specific protein may interact with the retroviral LTR and regulate transcription of genes under LTR control.
How do retroviral oncogenes induce transformation in avian erythroid cells?
The v-erb B oncogene, as well as other oncogenes of the src-gene family transform immature erythroid cells from chick bone marrow in vivo and in vitro, results in a differentiation arrest of the transformed cells, which now only use the self-renewal pathway.
Defective v-erbB genes can be complemented by v-erbA in erythroblast and fibroblast transformation.
The results show that the transforming activity of the mutants is gradually diminished, and completely abolished in those mutants that do not produce stable v-erbB proteins, suggesting that a larger part of the C-terminal domain is required for mitogenic signalling in erythroid cells than in fibroblasts.
A single point mutation in erbA restores the erythroid transforming potential of a mutant avian erythroblastosis virus (AEV) defective in both erbA and erbB oncogenes.
It is demonstrated that two co‐operating oncogenes, an active v‐erbA and a defectivev‐erbB, can transform a cell type not transformed by either oncogene alone, as well as a single amino acid substitution inactivated the td359 v-erbA protein and its reversion led to the reactivation of the protein.