Ghysdael J, Beug H
Institut-Curie, Section de Biologie, Orsay, France.
Cancer Surv. 1992;14:169-80.
The v-erbA oncogene of avian erythroblastosis virus alters the growth properties and arrests differentiation of chick erythroid progenitor cells. The v-erbA protein is a mutated, ligand independent version of the c-erbA/T3R alpha chick receptor for T3, a ligand dependent transcriptional regulator. In reconstituted systems using idealized hormone responsive elements, over-expressed v-erbA acts as a dominant repressor of transcription mediated by liganded c-erbA/T3R alpha. This property seems to account for at least part of the phenotype of AEV transformed erythroid cells and for the transcriptional repression of some erythrocyte specific genes. However, v-erbA is likely to interfere with regulatory circuits other than those directly regulated by T3 receptors. Aspects of this hypothesis are discussed in the context of available evidence for the role of T3 and other hormones in erythroid progenitor cells proliferation/differentiation.
禽成红细胞增多症病毒的v-erbA癌基因改变了鸡红细胞祖细胞的生长特性并阻止其分化。v-erbA蛋白是c-erbA/T3Rα鸡T3受体的一种突变的、不依赖配体的形式，T3受体是一种依赖配体的转录调节因子。在使用理想化激素反应元件的重组系统中，过表达的v-erbA作为由配体化的c-erbA/T3Rα介导的转录的显性阻遏物。这一特性似乎至少部分解释了AEV转化的红细胞的表型以及一些红细胞特异性基因的转录抑制。然而，v-erbA可能会干扰除了那些直接由T3受体调节的之外的其他调节回路。在关于T3和其他激素在红细胞祖细胞增殖/分化中的作用的现有证据的背景下，讨论了这一假说的各个方面。
