Abstract
The v-erbA oncogene of avian erythroblastosis virus (AEV) encodes an aberrant version of a gene for a thyroid hormone receptor (c-erbA) and functions in neoplasia by blocking erythroid differentiation and altering the growth properties of fibroblasts. The v-erbA gene has been proposed to act as a dominant negative allele, functioning by interfering with the actions of its normal cell homologs, the thyroid hormone receptors. The v-erbA protein can also, however, interfere with the actions of other members of the nuclear hormone receptor family, and it has been proposed that interference with a retinoic acid-mediated response may be a crucial determinant of v-erbA's function in the cancer cell. Here we report that the ability of v-erbA to interfere with retinoic acid receptor (RAR) action extends to the neoplastic erythroid cell and that v-erbA can inhibit transcriptional activation by all three isoforms (α, β, and γ) of RAR. Overexpression of RAR-α was found to partially overcome the presumptive v-erbA block to transcription in the erythroleukemic cell. These results are consistent with our hypothesis that v-erbA can act in neoplasia by interfering with a retinoic acid-mediated signal transduction pathway.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1067-1074 |
| Number of pages | 8 |
| Journal | Journal of Virology |
| Volume | 67 |
| Issue number | 2 |
| State | Published - Feb 1993 |
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ASJC Scopus subject areas
- Immunology
Cite this
v-erbA acts receptors on retinoic acid receptors in immature avian erythroid cells. / Sande, Stephen; Sharif, Mohammed; Chen, Hongwu; Privalsky, Martin.
In: Journal of Virology, Vol. 67, No. 2, 02.1993, p. 1067-1074.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - v-erbA acts receptors on retinoic acid receptors in immature avian erythroid cells
AU - Sande, Stephen
AU - Sharif, Mohammed
AU - Chen, Hongwu
AU - Privalsky, Martin
PY - 1993/2
Y1 - 1993/2
N2 - The v-erbA oncogene of avian erythroblastosis virus (AEV) encodes an aberrant version of a gene for a thyroid hormone receptor (c-erbA) and functions in neoplasia by blocking erythroid differentiation and altering the growth properties of fibroblasts. The v-erbA gene has been proposed to act as a dominant negative allele, functioning by interfering with the actions of its normal cell homologs, the thyroid hormone receptors. The v-erbA protein can also, however, interfere with the actions of other members of the nuclear hormone receptor family, and it has been proposed that interference with a retinoic acid-mediated response may be a crucial determinant of v-erbA's function in the cancer cell. Here we report that the ability of v-erbA to interfere with retinoic acid receptor (RAR) action extends to the neoplastic erythroid cell and that v-erbA can inhibit transcriptional activation by all three isoforms (α, β, and γ) of RAR. Overexpression of RAR-α was found to partially overcome the presumptive v-erbA block to transcription in the erythroleukemic cell. These results are consistent with our hypothesis that v-erbA can act in neoplasia by interfering with a retinoic acid-mediated signal transduction pathway.
AB - The v-erbA oncogene of avian erythroblastosis virus (AEV) encodes an aberrant version of a gene for a thyroid hormone receptor (c-erbA) and functions in neoplasia by blocking erythroid differentiation and altering the growth properties of fibroblasts. The v-erbA gene has been proposed to act as a dominant negative allele, functioning by interfering with the actions of its normal cell homologs, the thyroid hormone receptors. The v-erbA protein can also, however, interfere with the actions of other members of the nuclear hormone receptor family, and it has been proposed that interference with a retinoic acid-mediated response may be a crucial determinant of v-erbA's function in the cancer cell. Here we report that the ability of v-erbA to interfere with retinoic acid receptor (RAR) action extends to the neoplastic erythroid cell and that v-erbA can inhibit transcriptional activation by all three isoforms (α, β, and γ) of RAR. Overexpression of RAR-α was found to partially overcome the presumptive v-erbA block to transcription in the erythroleukemic cell. These results are consistent with our hypothesis that v-erbA can act in neoplasia by interfering with a retinoic acid-mediated signal transduction pathway.
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M3 - Article
C2 - 8093487
AN - SCOPUS:0027393961
VL - 67
SP - 1067
EP - 1074
JO - Journal of Virology
JF - Journal of Virology
SN - 0022-538X
IS - 2
ER -