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|Title:||Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2.|
|Citation:||Oncogene, 1997; 15(24):2885-2898|
|Abstract:||Primary murine fetal hemopoietic cells were transformed with a fusion protein consisting of the ligand-binding domain of the estrogen receptor and a carboxyl-terminally truncated c-Myb protein (ERMYB). The ERMYB-transformed hemopoietic cells exhibit an immature myeloid phenotype when grown in the presence of beta-estradiol. Upon removal of beta-estradiol, the ERMYB cells display increased adherence, decreased clonogenicity and differentiate to cells exhibiting granulocyte or macrophage morphology. The expression of the c-myc, c-kit, cdc2 and bcl-2 genes, which are putatively regulated by Myb, was investigated in ERMYB cells grown in the presence or absence of beta-estradiol. Neither c-myc nor cdc2 expression was down-regulated after removal of beta-estradiol demonstrating that differentiation is not a consequence of decreased transactivation of these genes by ERMYB. While bcl-2 expression was reduced by 50% in ERMYB cells grown in the absence of beta-estradiol, there was no increase in DNA laddering, suggesting that Myb was not protecting ERMYB cells from apoptosis. In contrast, a substantial (200-fold) decrease in c-kit mRNA level was observed following differentiation of ERMYB cells, and c-kit mRNA could be partially re-induced by the re-addition of beta-estradiol. Furthermore, a reporter construct containing the c-kit promoter was activated when cotransfected with a Myb expression vector, providing further evidence of a role for Myb in the regulation of c-kit.|
|Keywords:||Granulocytes; Hematopoietic Stem Cells; Cell Line, Transformed; Macrophages; Fetus; Animals; Mice, Inbred CBA; Mice; Retroviridae; Estradiol; Proto-Oncogene Proteins c-myb; Trans-Activators; Proto-Oncogene Proteins; Receptors, Estrogen; Recombinant Fusion Proteins; DNA; RNA, Messenger; Cell Division; Apoptosis; Cell Differentiation; Down-Regulation; Genes, cdc; Genes, myc; Genetic Vectors; Proto-Oncogene Proteins c-kit|
|Appears in Collections:||Medicine publications|
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