Myb binding sites within the N-ras promoter repress transcription

Transformation by v-Myb

“…Because v-Myb and c-Myb can act as transcriptional repressors as well as transcriptional activators (Ganter and Lipsick, 1997;Mizuguchi et al, 1995;Nakagoshi et al, 1989), these results raise the question of whether repression rather than activation of speci®c cellular genes might be critical for oncogenic transformation.…”

CDK-independent activities of D type cyclins

“…At ¢rst glance it appears counter-intuitive that an oncogenic transcription factor like v-Myb would be subject to negative regulation by a growth-promoting cyclin. However, in addition to their transactivating capacity, both c-Myb and v-Myb can also function as repressors of transcription [33]. In this respect, Myb proteins may resemble E2F transcription factors, which can also both activate and repress transcription.…”

The carbonic anhydrase I locus contains a c-Myb target promoter and modulates differentiation of murine erythroleukemia cells

“…However, it is unclear if these genes play a role in mediating v-Myb transformation of myeloid cells. Second, several candidate c-Myb-regulated genes have been identified based on the presence of Myb consensus DNA-binding sequences in the 5 0 flanking regions including genes encoding c-kit (Ratajczak et al, 1998), human CD34 , CD13/aminopeptidase N (Shapiro, 1995), human oxytocin receptor (Inoue et al, 1994), murine neutrophil elastase (Oelgeschlager et al, 1996;Nuchprayoon et al, 1997), mouse CD4 (Siu et al, 1992), c-Myc (Evans et al, 1990;Schmidt et al, 2000) and N-Ras (Ganter and Lipsick, 1997), although in some cases little evidence has been presented demonstrating the ability of c-Myb to regulate expression of the endogenous locus. Finally, microarray assays have been used to identify potential c-Myb target promoters in models based on forced expression of Myb family members or a dominant interfering Myb protein (Rushton et al, 2003;Lang et al, 2005).…”