Document Detail

c-Myb function in fibroblasts.
MedLine Citation:
PMID:  9369944     Owner:  NLM     Status:  MEDLINE    
The protooncogene c-myb is a nuclear transcription factor that shares significant sequence homology with two other myb family members, A-myb and B-myb. Recent studies have suggested that c-myb is involved in regulation of the cell cycle via control of intracellular calcium [Ca2+]i concentration. Given the limited cell type expression of the c-myb gene, we set out to investigate whether myb-dependent cell cycle regulation occurs in cells not known to express the c-myb protein. NIH 3T3 fibroblasts were stably transfected with an inducible c-myb dominant negative construct composed of a myb DNA binding domain linked to the Drosophila engrailed transcription suppresser (pGREMEn) and a full-length murine c-myb cDNA sequence. Induced expression of the dominant negative construct was associated with a G1 cell cycle arrest and a failure to increase late G1 intracellular calcium levels. Similar expression studies in mouse embryonic fibroblasts derived from the c-myb knockout mouse have demonstrated lower baseline [Ca2+]i levels than in normal mice fibroblasts that were not further lowered by MEn expression. We conclude that regulation of calcium homeostasis and cell cycle progression via myb-dependent transcription may play an important role in cells not possessing detectable levels of c-myb protein.
K Bein; M Husain; J A Ware; M L Mucenski; R D Rosenberg; M Simons
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  173     ISSN:  0021-9541     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1997-12-04     Completed Date:  1997-12-04     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  319-26     Citation Subset:  IM    
Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
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MeSH Terms
3T3 Cells
Calcium / metabolism
Cell Cycle / physiology*
Cells, Cultured
Cytoplasm / metabolism
DNA-Binding Proteins / biosynthesis
Embryo, Mammalian
Embryo, Nonmammalian
Homeodomain Proteins / biosynthesis
Mice, Knockout
Proto-Oncogene Proteins / biosynthesis,  physiology*
Proto-Oncogene Proteins c-myb
Recombinant Fusion Proteins / biosynthesis
Trans-Activators / biosynthesis,  physiology*
Transcription Factors*
Transcription, Genetic
Grant Support
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Homeodomain Proteins; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-myb; 0/Recombinant Fusion Proteins; 0/Trans-Activators; 0/Transcription Factors; 0/engrailed homeobox proteins; 7440-70-2/Calcium

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