v-Myb represses the transcription of Ets-2

MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal cancer

“…Every coin has two sides, and the transcription factor MYB, also known as a proto-oncogene, operates as a transcriptional activator as well as transcriptional repressor. [30][31][32][33] Hitherto, some evidence has strengthened the case that MYB can transactivate Bcl-2 by recognizing the transcription factor binding site (TFBS). 34,35 More excitingly, the data from our study revealed that MYB functions as a transcriptional repressor by inhibiting miR-148a, which could also silence Bcl-2.…”

Genomic tools for dissecting oncogenic transcriptional networks in human leukemia

“…13 This approach has been extended to the analysis of additional transcription factors by generating fusions turning them into estrogen-activated proteins by fusion with the hormone-binding domain of the estrogen receptor. [14][15][16][17] Alternatively, a loss-offunction variation of this approach can be achieved by inactivation of the transcription factor of interest by expression of a dominant negative form of the protein or by RNA interference knockdown. 18,19 Despite the success of these approaches in the identification of relevant target genes for oncogenic transcription factors, their use has been limited by several technical caveats, including the need to express exogenous and structurally modified versions of the protein of interest and the broad biological effects of cycloheximide treatment.…”

MYB IS Required for B-Selection During Thymopoises

“…Upon examination of the lists of genes that were up or down regulated in c-Myb deficient and sufficient thymocytes, we identified a number of genes previously reported as c-Myb transcriptional targets in other cell types and model systems including Nras [326], Vcl [154], CD53 [256], Cdkn1a [154], Cbx4 [256], Ets2 [327], Bcl2 [232,233,256,328], and Itga4 [304]. However, only Cbx4 and Bcl2 were reported to be direct c-Myb targets as demonstrated by a ChIP of endogenous c-Myb from promoters in a multipotent hematopoietic cell line FDCP-mix [256].…”