Document Detail

A-myb is expressed in bovine vascular smooth muscle cells during the late G1-to-S phase transition and cooperates with c-myc to mediate progression to S phase.
MedLine Citation:
PMID:  9111313     Owner:  NLM     Status:  MEDLINE    
The Myb family of transcription factors is defined by homology within the DNA binding domain and includes c-Myb, A-Myb, and B-Myb. The protein products of the myb genes all bind the Myb-binding site (MBS) [YG(A/G)C(A/C/G)GTT(G/A)]. A-myb has been found to display a limited pattern of expression. Here we report that bovine aortic smooth muscle cells (SMCs) express A-myb. Sequence analysis of isolated bovine A-myb cDNA clones spanning the entire coding region indicated extensive homology with the human gene, including the putative transactivation domain. Expression of A-myb was cell cycle dependent; levels of A-myb RNA increased in the late G1-to-S phase transition following serum stimulation of serum-deprived quiescent SMC cultures and peaked in S phase. Nuclear run-on analysis revealed that an increased rate of transcription can account for most of the increase in A-myb RNA levels. Treatment of SMC cultures with 5,6-dichlorobenzimidazole riboside, a selective inhibitor of RNA polymerase II, indicated an approximate 4-h half-life for A-myb mRNA during the S phase of the cell cycle. Expression of A-myb by SMCs was stimulated by basic fibroblast growth factor, in a cell density-dependent fashion. Cotransfection of a human A-myb expression vector activated a multimerized MBS element-driven reporter construct approximately 30-fold in SMCs. The activity of c-myb and c-myc promoters, which both contain multiple MBS elements, were similarly transactivated, approximately 30- and 50-fold, respectively, upon cotransfection with human A-myb. Lastly, A-myb RNA levels could be increased by a combination of phorbol ester plus insulin-like growth factor 1. To test the role of myb family members in progression through the cell cycle, we comicroinjected c-myc and myb expression vectors into serum-deprived quiescent SMCs. The combination of c-myc and either A-myb or c-myb but not B-myb synergistically led to entry into S phase, whereas microinjection of any vector alone had little effect on S phase entry. Thus, these results suggest that A-myb is a potent transactivator in bovine SMCs and that its expression induces progression into S phase of the cell cycle.
D J Marhamati; R E Bellas; M Arsura; K E Kypreos; G E Sonenshein
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Molecular and cellular biology     Volume:  17     ISSN:  0270-7306     ISO Abbreviation:  Mol. Cell. Biol.     Publication Date:  1997 May 
Date Detail:
Created Date:  1997-05-15     Completed Date:  1997-05-15     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  8109087     Medline TA:  Mol Cell Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2448-57     Citation Subset:  IM    
Department of Biochemistry, Boston University School of Medicine, Massachusetts 02118, USA.
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MeSH Terms
Base Sequence
DNA, Complementary / chemistry,  isolation & purification
Fibroblast Growth Factor 2 / metabolism
G1 Phase
Molecular Sequence Data
Muscle, Smooth, Vascular / metabolism*
Proto-Oncogene Proteins / metabolism*
Proto-Oncogene Proteins c-myc / metabolism*
RNA, Messenger / metabolism
S Phase
Trans-Activators / metabolism*
Grant Support
Reg. No./Substance:
0/DNA, Complementary; 0/MYBL1 protein, human; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-myc; 0/RNA, Messenger; 0/Trans-Activators; 103107-01-3/Fibroblast Growth Factor 2

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