The c-myb proto-oncogene has repeatedly been a target of retroviral insertional mutagenesis in murine and avian haemopoietic neoplasms. The most common mechanism by which avian and murine retroviruses activate c-myb’s oncogenic potential is promoter insertional mutagenesis where the viral LTR function replaces the endogenous transcriptional control resulting in constitutive expression of the myb mRNA. Another mechanism of activation of c-Myb is achieved through the integration of retroviruses into the 3’ region of the c-myb locus. The 3’ untranslated region is replaced with viral polyA causing an increased stability of the c-myb mRNA. In addition, this type of activation results in the carboxyl-terminal truncation of the c-Myb protein providing increased proteolytic stability and transactivation capacity. Several virus integration sites were also mapped within the genomic region surrounding the c-myb locus suggesting that retrovirus integrations outside of the coding region can also impose activation via the long-range effect of retroviral regulatory elements.
Chapter PDF
Similar content being viewed by others
Keywords
- Insertional Mutagenesis
- Mixed Lineage Leukaemia
- Haemopoietic Cell
- Transactivation Capacity
- Negative Regulatory Domain
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2004 Kluwer Academic Publishers
About this chapter
Cite this chapter
Bies, J., Wolff, L. (2004). C-Myb And Leukaemogenesis. In: Frampton, J. (eds) Myb Transcription Factors: Their Role in Growth, Differentiation and Disease. Proteins and Cell Regulation, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-2869-4_16
Download citation
DOI: https://doi.org/10.1007/978-1-4020-2869-4_16
Publisher Name: Springer, Dordrecht
Print ISBN: 978-1-4020-2779-6
Online ISBN: 978-1-4020-2869-4
eBook Packages: Springer Book Archive