v-jun cooperates with v-erbB to transform the thrombocytic/megakaryocytic lineage.
AUTOR(ES)
Garcia, M
RESUMO
The transforming properties of v-jun, the viral counterpart of the transcription factor AP1, were investigated in avian hematopoietic cells. Two retroviruses, called JB and JBN, expressing both v-jun and v-erbB, were constructed using an avian erythroblastosis-based vector. We show that the cooperative action of both oncogenes allowed the virus to efficiently transform bone marrow cells. No such transformation was obtained with either oncogene alone. JB-transformed bone marrow cells expressed GATA-1, TAL-1, and histone H5, suggesting that they belong to the erythrocytic/thrombocytic lineage. (Thrombocytes are the avian homologues of mammal megakaryocytes.) Moreover, after induction with phorbol 12-myristate 13-acetate JB-transformed bone marrow cells began to differentiate and synthesized high levels of platelet glycoproteins, indicating that they were of thrombocytic origin. These results were confirmed by c-ets1 analysis since this transcription factor, specifically found in cells with megakaryocytic but not erythrocytic features, was clearly detected in these cells.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=47455Documentos Relacionados
- Cooperation of v-jun and v-erbB oncogenes in embryo fibroblast transformation in vitro and in vivo.
- The v-erbB oncogene confers enhanced cellular susceptibility to reovirus infection.
- Transcription Factor ATF2 Cooperates with v-Jun To Promote Growth Factor-Independent Proliferation In Vitro and Tumor Formation In Vivo
- Ligand-independent dimerization of oncogenic v-erbB products involves covalent interactions.
- Dissecting the activating mutations in v-erbB of avian erythroblastosis virus strain R.