Transformation by v-Myb

Lipsick, Joseph S.; Wang, Duen-Mei

doi:10.1038/sj.onc.1202745

Cited by 147 publications

(116 citation statements)

References 133 publications

Supporting

Mentioning

111

Contrasting

Unclassified

Order By: Relevance

“…As presented in Figure 8c, ectopic overexpression of CAI protein in clone 4-1(S) did not alter proliferation in logarithmically growing C19 MEL cells as compared to the empty vector stable transfectant or parental C19 MEL cells. When differentiation was induced in the empty vector stable transfectant or the parental C19 cell line, proliferation began to decrease between days 2 and 3 after treatment with HMBA, which is consistent with numerous previous reports Lipsick, 1996). However, in contrast, we found little decrease in proliferation of the clone 4-1(S) stable transfectant cells in response to HMBA, suggesting that maintenance of CAI expression is associated with a proliferating state in C19 MEL cells.…”

Section: Caie Function Is Dependent On Myb Activity In Mel Cellssupporting

confidence: 92%

See 1 more Smart Citation

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

2006

View full text Add to dashboard Cite

Section: Caie Function Is Dependent On Myb Activity In Mel Cellssupporting

confidence: 92%

“…The v-and c-Myb proteins are nuclear, DNA-binding phosphoproteins that function as transcription activators (Lipsick, 1996). Three distinct functional domains have been identified on c-Myb: a DNA-binding domain (DBD), a transactivation domain (TA) and a negative regulatory domain (NRD) (Oh and Reddy, 1999).…”

Section: Introductionmentioning

confidence: 99%

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

2006

View full text Add to dashboard Cite

“…It also harbors 10 point mutations with respect to c-Myb in different domains of the protein (Fig. 1A); together, the truncations and point mutations contribute to its oncogenic activation in avian systems at least (27,28). There are four DBD point mutations, three of which constitute what we have termed the 3M mutations.…”

Section: Introductionmentioning

confidence: 99%

Mutations in Multiple Domains of c-Myb Disrupt Interaction with CBP/p300 and Abrogate Myeloid Transforming Ability

Pattabiraman

Sun

Dowhan

et al. 2009

Molecular Cancer Research

View full text Add to dashboard Cite

The c-myb proto-oncogene is a key regulator of hematopoietic cell proliferation and differentiation. MYB mRNA is expressed at high levels in, and is required for the proliferation of, most human myeloid and acute lymphoid leukemias. Recently, chromosomal translocation and genomic duplications of c-MYB have been identified in human T-cell acute leukemia. The present work focuses on the effects of mutations in different domains of the murine c-Myb protein on its transforming ability as defined by suppression of myelomonocytic differentiation and continued proliferation. Using both a novel myeloid cell line-based assay and a primary hematopoietic cell assay, we have shown that mutation of single residues in the transactivation domain important for CBP/p300 binding leads to complete loss of transforming ability. We also simultaneously mutated residues in the DNA-binding domain and the negative regulatory domain of the protein. These double mutants, but not the corresponding single mutants, show a complete loss of transforming activity. Surprisingly, these double mutants show severely impaired transactivation and are also defective for CBP/ p300 binding. Our results imply that multiple Myb domains influence its interaction with CBP/p300, highlight the importance of this interaction for myeloid transformation, and suggest an approach for molecular targeting

show abstract

“…The c-myb proto-oncogene encodes a sequence-speci®c DNA binding protein containing three homeo domainrelated DNA binding repeats (repeats 1, 2 and 3) (Lipsick, 1996;Ness, 1996). c-Myb is thought to regulate the growth and di erentiation of immature hematopoietic cells since adult-type hematopoiesis in homozygous c-myb mutant mice is greatly impaired (Mucenski et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory interaction of c-Myb and GATA-1 via transcriptional co-activator CBP

et al. 2000

View full text Add to dashboard Cite

Gene targeting experiments have revealed that transcription factors such as c-Myb and GATA-1 play crucial roles during hematopoietic di erentiation. c-Myb is necessary in the immature cells of almost every hematopoietic lineage and GATA-1 is essential for the development of the erythroid lineage. In addition, CREB-binding protein (CBP) acts as a transcriptional adapter for various transcription factors, including cMyb and GATA-1. In this paper, we show that the transcription factors c-Myb and GATA-1 each inhibit the transcriptional activity of the other and that any possible bipartite complexes c-Myb, GATA-1, and CBP could be formed, but the tripartite complex was hardly formed. The exclusive binding of GATA-1 and c-Myb to CBP is probably the molecular basis for the mutual inhibition of their transcriptional activity. Our data suggest that cross-talk between these three factors might be important for hematopoietic di erentiation and that CBP functions as a key molecule during the process.

show abstract

Transformation by v-Myb

Cited by 147 publications

References 133 publications

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

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

Mutations in Multiple Domains of c-Myb Disrupt Interaction with CBP/p300 and Abrogate Myeloid Transforming Ability

Inhibitory interaction of c-Myb and GATA-1 via transcriptional co-activator CBP

Contact Info

Product

Resources

About