Transcriptional activation by the v-myb oncogene and its cellular progenitor, c-myb

Weston, Kathleen; Bishop, J. Michael

doi:10.1016/0092-8674(89)90405-4

Cited by 288 publications

(194 citation statements)

References 42 publications

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“…Similar studies of the human promoter identified a PU.1-responsive element around 170 bp upstream from the start codon that activated transcription in nonmacrophages and was essential for maximal expression in macrophages (15). The c-myb gene also encodes a DNA binding protein that acts as a transcriptional activator (16)(17)(18)(19)(20). The c-myb product is expressed primarily in hematopoietic cells (21) and is essential for the normal differentiation.…”

mentioning

confidence: 85%

Opposing actions of c-ets/PU.1 and c-myb protooncogene products in regulating the macrophage-specific promoters of the human and mouse colony-stimulating factor-1 receptor (c-fms) genes.

Reddy

Yang

Xie

et al. 1994

The Journal of Experimental Medicine

113

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The receptor for macrophage colony stimulating factor (CSF-1), the c-fms gene product, is a key determinant in the differentiation of monocytic phagocytes. Dissection of the human and mouse c-fms proximal promoters revealed opposing roles for nuclear protooncogenes in the transcriptional regulation of this gene. On the one hand, c-ets-1, c-ets-2, and the macrophage-specific factor PU.1, but not the ets-factor PEA3, trans-activated the c-fms proximal promoter. On the other hand c-myb repressed proximal promoter activity in macrophages and blocked the action of c-ets-1 and c-ets-2. Basal c-fms promoter activity was almost undetectable in the M1 leukaemia line, which expressed high levels of c-myb, but was activated as cells differentiated in response to leukemia inhibitory factor and expressed c-fms mRNA. The repressor function of c-myb depended on the COOH-terminal domain of the protein. We propose that ets-factors are necessary for the tissue-restricted expression of c-fms and that c-myb acts to ensure correct temporal expression of c-fms during myeloid differentiation.

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mentioning

confidence: 85%

Opposing actions of c-ets/PU.1 and c-myb protooncogene products in regulating the macrophage-specific promoters of the human and mouse colony-stimulating factor-1 receptor (c-fms) genes.

Reddy

Yang

Xie

et al. 1994

The Journal of Experimental Medicine

113

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“…Both artificial promoter constructs containing Myb-binding sites [26,30,44] transcriptional activation, and negative regulation, respectively [35]. The negative regulatory domain (NRD), located in the carboxyl-proximal portion of the molecule, is important for modulation of c-Myb activity.…”

Section: Introductionmentioning

confidence: 99%

Human A‐myb gene encodes a transcriptional activator containing the negative regulatory domains

Takahashi

Nakagoshi²,

Sarai³

et al. 1995

FEBS Letters

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The myb gene family has three members, c-myb, A-myb, and B-myb. A-myb mRNA is mainly expressed in testis and peripheral blood leukocytes. A-Myb can activate transcription from the promoter containing Myb-binding sites in all cells examined. In addition to the two domains (a DNA-binding domain and a transcriptional activation domain), two negative regulatory domains have been identified in A-Myb. These results indicate that A-Myb functions as a transcriptional activator mainly in testis and peripheral blood cells, and the regulatory mechanism of A-Myb activity is similar to that of c-Myb.

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“…The v-Myb and Myb genes encode nuclear DNA binding proteins that function as both transcriptional activators and repressors [134][135][136]. c-Myb is highly evolutionarily conserved and is found in all vertebrates examined [137].…”

Section: C-mybmentioning

confidence: 99%

“…Deletion of carboxylterminal regions from c-Myb and testing the transactivation activity in transient DNA transfection assays resulted in a ten-fold increase in transcriptional transactivation activity [135,141]. Interestingly, yeast two-hybrid studies revealed that the amino and carboxyl-termini of c-Myb interact with one another via the first 192 amino acids of the amino-terminal portion of c-Myb containing the DBD and a highly conserved carboxyl terminal region referred to as the EVES motif [157].…”

Section: C-mybmentioning

confidence: 99%

“…The TAD was identified by fusing a Gal4 DBD with portions of c-Myb and testing the ability of the fusion protein to activate a promoter with a Gal4 binding site linked to a reporter gene [135,153]. Little is known about the requirements of this domain but point mutations suggest that acidity of the residues is not essential and conformation is of critical importance [135]. In addition, recent studies demonstrated that undefined regulatory elements within the transactivation domain control promoter specific target gene expression [154].…”

Section: C-mybmentioning

confidence: 99%

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MYB IS Required for B-Selection During Thymopoises

Duley¹

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Abstractc-Myb is a transcription factor required during hematopoiesis and is crucial for multiple stages of thymopoiesis. Understanding c-Myb function during hematopoiesis has been greatly impeded due to the lack of a tractable genetic system. We have used the Cre/loxP approach to conditional mutagenesis to study c-Myb function during thymopoiesis. Thymocyte specific inactivation of the Myb locus demonstrated a block in DN3 to DN4 differentiation concomitant with impaired Vβ to DJβ recombination of the Tcrb locus suggesting that the inability to generate a TCRβ protein blocked DN3 differentiation. However, some DN3 thymocytes

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Transcriptional activation by the v-myb oncogene and its cellular progenitor, c-myb

Cited by 288 publications

References 42 publications

Opposing actions of c-ets/PU.1 and c-myb protooncogene products in regulating the macrophage-specific promoters of the human and mouse colony-stimulating factor-1 receptor (c-fms) genes.

Opposing actions of c-ets/PU.1 and c-myb protooncogene products in regulating the macrophage-specific promoters of the human and mouse colony-stimulating factor-1 receptor (c-fms) genes.

Human A‐myb gene encodes a transcriptional activator containing the negative regulatory domains

MYB IS Required for B-Selection During Thymopoises

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