Molecular characterization of three erbB transducing viruses generated during avian leukosis virus-induced erythroleukemia: extensive internal deletion near the kinase domain activates the fibrosarcoma- and hemangioma-inducing potentials of erbB.

摘要: Three new erbB transducing viruses generated during avian leukosis virus-induced erythroblastosis have been cloned and sequenced, their transforming abilities analyzed. Provirus 9134 E1 expresses an amino-terminally truncated product that is analogous to the proviral insertionally activated c-erbB gag-erbB fusion product. This virus efficiently induces erythroblastosis, but does not transform fibroblasts in vitro or induce sarcomas vivo. In contrast, S3 identical of E1, with exception a large internal deletion located between kinase domain putative autophosphorylation site, P1. Interestingly, this no longer capable inducing can both fibrosarcomas hemangiomas F3 has sustained approximately 23-amino-acid carboxy-terminal truncation sarcomagenesis. shortest sufficient reveal sarcomagenic potential protein. The distinct properties these indicate different structural domains confer disease specificities.