Skip Navigation

This Article
Right arrow Print PDF (1864K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Sobieszczuk, P. W.
Right arrow Articles by Dunn, A. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sobieszczuk, P. W.
Right arrow Articles by Dunn, A. R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1989, Vol. 17, No. 23 9593-9611
© 1989

MOLECULAR BIOLOGY

Structure and biological activity of the transcriptional initiation sequences of the murine c-myb oncogene

Peter W. Sobieszczuk*, Thomas J. Gonda and Ashley R. Dunn

Ludwig Institute for Cancer Research, Melbourne Branch of Tumor Biology, PO Royal Melbourne Hospital Parkville, Victoria 3050, Australia

*To whom correspondence should be addressed at Centre for Early Human Development, Monash Medical Centre, 246 Clayton Rd., Clayton, Victoria 3168, Australia

Received September 15, 1989. Accepted November 9, 1989.

To study the control mechanism(s) that govern the transcription of c-myb, genomic clones corresponding to the 5' region of the murine c-myb gene have been isolated and characterized structurally and functionally. Primer extension and nuclease protection analysis have revealed the presence of multiple transcriptional initiation sites, that are utilized in several hemopoietic cell lines (WEHI3B(D+), FDC-P1 and RB22.2). Some of the sites are used in all cell lines but others are unique; all are located in a region of the c-myb gene that is G-C rich, contains a number of potential Sp1 binding sites and lacks classical promoter consensus sequences.

Experiments in which well characterized promoters controlling expression of a reporter gene have been replaced by fragments of c-myb DNA (including the observed cap sites) were performed in an attempt to demonstrate promoter activity in various cell types. It was shown that a region of the c-myb gene (approximately 1.0 kbp upstream from the splice donor site of the first exon) contains a weak promoter that has a low level of transcriptional activity in hemopoietic as well as in fibroblastic cells. These results support the suggestion that c-myb expression is not regulated primarily at the level of initiation of transcription.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 BloodHome page
T. Bellon, D. Perrotti, and B. Calabretta
Granulocytic Differentiation of Normal Hematopoietic Precursor Cells Induced by Transcription Factor PU.1 Correlates With Negative Regulation of the c-myb Promoter
Blood, September 1, 1997; 90(5): 1828 - 1839.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Schaefer, M. Magocsi, U. Stocker, A. Fandrich, and H. Marquardt
Ca2+/Calmodulin-dependent and -independent Down-regulation of c-myb mRNA Levels in Erythropoietin-responsive Murine Erythroleukemia Cells. THE ROLE OF CALCINEURIN
J. Biol. Chem., June 7, 1996; 271(23): 13484 - 13490.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. R. Toth, R. F. Hostutler, A. S.:Jr. Baldwin, and T. P. Bender
Members of the Nuclear Factor kappaB Family Transactivate the Murine c-myb Gene
J. Biol. Chem., March 31, 1995; 270(13): 7661 - 7671.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.