Can Pim-1 convert c-Myb into an oncogene?
Just as c-Myb activation may not be the sole factor in pim-1-mediated transformation, Pim-1 expression may not be sufficient to oncogenically activate c-Myb. The activity of c-Myb protein is tightly regulated at all levels, and many of these regulatory limitations have been lost in the original avian v-Myb oncoprotein: c-myb mRNA is short-lived and is only made during G1 phase of the cell cycle in many cell types (reviewed in Weston, 1998), whilst v-myb mRNA must be overexpressed for transformation to occur (Schirm et al., 1990); c-Myb protein is also short-lived, whilst v-Myb is not (Bies and Wolff, 1997); c-Myb contains binding sites for a number of negative regulatory molecules, most of which do not bind v-Myb (Ness, 1999), and finally, the truncations found in the v-Myb oncogene affect regions of the protein involved in its phosphorylation by kinases other than Pim-1 (Aziz et al., 1993; Luscher et al., 1990). In mice, the minimal requirements for oncogenic activation of c-Myb appea
