The Conserved DNA Binding Domain Mediates Similar Regulatory Interactions for A-Myb, B-Myb, and c-Myb Transcription Factors

Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb

“…The binding was efficiently competed by excess specific but not nonspecific oligonucleotides and could be super-shifted using anti-Myb antibodies (data not shown). These results agree with several published studies showing that c-Myb and v-Myb have similar in vitro DNA binding activities (Ness et al, 1989;Leverson and Ness, 1998;Rushton and Ness, 2001). In transient transfection assays, each of the Myb proteins strongly activated a reporter gene construct containing several Myb binding sites cloned upstream of a minimal promoter driving expression of luciferase as well as other reporter genes containing Myb-regulated promoters (e.g.…”

MicroRNA-548c-3p inhibits T98G glioma cell proliferation and migration by downregulating c-Myb

“…The proto-oncogene c-Myb (c-Myb) codes for a transcription factor that is a member of the Myb family (16,17). The MicroRNA-548c-3p inhibits T98G glioma cell proliferation and migration by downregulating c-Myb transcription factor Myb has a key role in stem and progenitor cell regulation within the colonic crypts, bone marrow and a neurogenic region of the adult brain (16).…”

Alternative RNA Splicing Produces Multiple Forms of c-Myb with Unique Transcriptional Activities

“…All the Myb proteins are structurally similar and have nearly identical DNA binding domains near their N termini, but they are more divergent in their central transcriptional activation domains and Cterminal negative regulatory domains. Although c-Myb, AMyb, and B-Myb can bind the same DNA sequences and activate the same promoters in reporter gene assays (31), the three proteins are differentially expressed, and mouse knockout experiments have shown that they have different biological roles (23,36,37). In addition, microarray assays showed that each protein activates a unique set of genes in human cells (30), and the differences in the activities of these proteins have been mapped primarily to differences in their unique transcriptional activation and C-terminal domains (18).…”