This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Campanero, M. R.
Right arrow Articles by Flemington, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Campanero, M. R.
Right arrow Articles by Flemington, E.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, December 1999, p. 8442-8450, Vol. 19, No. 12
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Distinct Cellular Factors Regulate the c-myb Promoter through Its E2F Element

Miguel R. Campanero, Monica Armstrong, and Erik Flemington*

Harvard University and Dana-Farber Cancer Institute, Boston, Massachusetts 02115

Received 11 February 1999/Returned for modification 31 March 1999/Accepted 30 August 1999

Most E2F-driven promoters are transiently activated around the G1/S transition. Although the promoter for the c-myb proto-oncogene harbors an E2F element, it is induced early in G1 following entry into the cell cycle. Furthermore, this promoter remains active throughout subsequent cell cycles. Since E2F sites function as repressor elements during G1 (due to the association of pRb with E2F factors), we investigated whether the E2F element in the c-myb promoter is regulated differently than E2F elements in promoters that are repressed during G1. By gel shift analysis, the E2F element from the c-myb promoter was found to form a unique complex, referred to as E2Fmyb-sp, which was not observed with E2F elements from several other promoters. Antibodies to DP-1, E2F1 to -5, p107, or pRb failed to either supershift or block E2Fmyb-sp complex formation. Methylation interference experiments indicate that the DNA contact residues for the E2Fmyb-sp complex are distinct from but overlapping with residues required for the binding of E2F proteins. In addition to the identification of E2Fmyb-sp, we have found that SP-1 binds to the c-myb E2F element. Functional studies revealed that E2Fmyb-sp and/or SP-1 are required to achieve full activation of the c-myb promoter in different cell types and to maintain elevated expression of the c-myb promoter during G1 in NIH 3T3 cells. These studies demonstrate that E2F elements can be regulated differently through the binding of unique sets of proteins.

* Corresponding author. Mailing address: Harvard University and Dana-Farber Cancer Institute, 44 Binney St., Boston, MA 02115. Phone: (617) 632-3852. Fax: (617) 632-2662. E-mail: erik_flemington{at}dfci.harvard.edu.

Molecular and Cellular Biology, December 1999, p. 8442-8450, Vol. 19, No. 12
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Molina-Privado, I., Rodriguez-Martinez, M., Rebollo, P., Martin-Perez, D., Artiga, M.-J., Menarguez, J., Flemington, E. K., Piris, M. A., Campanero, M. R. (2009). E2F1 Expression Is Deregulated and Plays an Oncogenic Role in Sporadic Burkitt's Lymphoma. Cancer Res. 69: 4052-4058 [Abstract] [Full Text]  
  • Alvaro-Blanco, J., Martinez-Gac, L., Calonge, E., Rodriguez-Martinez, M., Molina-Privado, I., Redondo, J. M., Alcami, J., Flemington, E. K., Campanero, M. R. (2009). A novel factor distinct from E2F mediates C-MYC promoter activation through its E2F element during exit from quiescence. Carcinogenesis 30: 440-448 [Abstract] [Full Text]  
  • Montanuy, I., Torremocha, R., Hernandez-Munain, C., Sune, C. (2008). Promoter Influences Transcription Elongation: TATA-BOX ELEMENT MEDIATES THE ASSEMBLY OF PROCESSIVE TRANSCRIPTION COMPLEXES RESPONSIVE TO CYCLIN-DEPENDENT KINASE 9. J. Biol. Chem. 283: 7368-7378 [Abstract] [Full Text]  
  • Davis, J. N., McCabe, M. T., Hayward, S. W., Park, J. M., Day, M. L. (2005). Disruption of Rb/E2F Pathway Results in Increased Cyclooxygenase-2 Expression and Activity in Prostate Epithelial Cells. Cancer Res. 65: 3633-3642 [Abstract] [Full Text]  
  • Davidson, C. J., Tirouvanziam, R., Herzenberg, L. A., Lipsick, J. S. (2005). Functional Evolution of the Vertebrate Myb Gene Family: B-Myb, but Neither A-Myb nor c-Myb, Complements Drosophila Myb in Hemocytes. Genetics 169: 215-229 [Abstract] [Full Text]  
  • Lin, Z., Yin, Q., Flemington, E. (2004). Identification of a Negative Regulatory Element in the Epstein-Barr Virus Zta Transactivation Domain That Is Regulated by the Cell Cycle Control Factors c-Myc and E2F1. J. Virol. 78: 11962-11971 [Abstract] [Full Text]  
  • Martinez-Gac, L., Marques, M., Garcia, Z., Campanero, M. R., Carrera, A. C. (2004). Control of Cyclin G2 mRNA Expression by Forkhead Transcription Factors: Novel Mechanism for Cell Cycle Control by Phosphoinositide 3-Kinase and Forkhead. Mol. Cell. Biol. 24: 2181-2189 [Abstract] [Full Text]  
  • Konishi, Y., Bonni, A. (2003). The E2F-Cdc2 Cell-Cycle Pathway Specifically Mediates Activity Deprivation-Induced Apoptosis of Postmitotic Neurons. J. Neurosci. 23: 1649-1658 [Abstract] [Full Text]  
  • Lauder, A., Castellanos, A., Weston, K. (2001). c-myb Transcription Is Activated by Protein Kinase B (PKB) following Interleukin 2 Stimulation of T Cells and Is Required for PKB-Mediated Protection from Apoptosis. Mol. Cell. Biol. 21: 5797-5805 [Abstract] [Full Text]  
  • Thykjaer, T., Workman, C., Kruhøffer, M., Demtröder, K., Wolf, H., Andersen, L. D., Frederiksen, C. M., Knudsen, S., Ørntoft, T. F. (2001). Identification of Gene Expression Patterns in Superficial and Invasive Human Bladder Cancer. Cancer Res. 61: 2492-2499 [Abstract] [Full Text]  
  • Campanero, M. R., Armstrong, M. I., Flemington, E. K. (2000). CpG methylation as a mechanism for the regulation of E2F activity. Proc. Natl. Acad. Sci. USA 97: 6481-6486 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»