Document Detail

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.
MedLine Citation:
PMID:  9416832     Owner:  NLM     Status:  MEDLINE    
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.
A Hogg; S Schirm; H Nakagoshi; P Bartley; S Ishii; J M Bishop; T J Gonda
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncogene     Volume:  15     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1998-01-15     Completed Date:  1998-01-15     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2885-98     Citation Subset:  IM    
Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Adelaide, South Australia.
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MeSH Terms
Cell Differentiation / drug effects,  genetics
Cell Division / drug effects
Cell Line, Transformed
DNA / biosynthesis,  chemistry
Down-Regulation / genetics*
Estradiol / deficiency,  physiology
Genes, cdc*
Genes, myc*
Genetic Vectors / chemical synthesis
Granulocytes / cytology*
Hematopoietic Stem Cells
Macrophages / cytology*
Mice, Inbred CBA
Proto-Oncogene Proteins / biosynthesis,  genetics*,  metabolism
Proto-Oncogene Proteins c-kit / genetics*
Proto-Oncogene Proteins c-myb
RNA, Messenger / biosynthesis,  chemistry
Receptors, Estrogen / biosynthesis,  genetics*,  metabolism
Recombinant Fusion Proteins / biosynthesis,  metabolism*
Retroviridae / genetics
Trans-Activators / biosynthesis,  genetics*,  metabolism
Reg. No./Substance:
0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-myb; 0/RNA, Messenger; 0/Receptors, Estrogen; 0/Recombinant Fusion Proteins; 0/Trans-Activators; 50-28-2/Estradiol; 9007-49-2/DNA; EC Proteins c-kit

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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