CBP as a transcriptional coactivator of c-Myb.

Dai, Ping; Akimaru, Hiroshi; Tanaka, Yasunori; Hou, De‐Xing; Yasukawa, Takashi; Kanei-Ishii, Chie; Takahashi, Tomomi; Ishii, Shunsuke

doi:10.1101/gad.10.5.528

Cited by 337 publications

(284 citation statements)

References 54 publications

(64 reference statements)

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“…Although Myb and CREB bind the same domain of CBP (Dai et al, 1996;Kiewitz and Wolfes, 1997;OelgeschlaÈ ger et al, 1996), the interaction with Myb proteins is constitutive rather than phosphorylation-dependent (Dai et al, 1996;OelgeschlaÈ ger et al, 1996). Interestingly, CBP and p300 can also interact with and stimulate the activity of C/EBPb (Mink et al, 1997;OelgeschlaÈ ger et al, 1996), suggesting that the coactivators may act as a bridge between Myb and C/EBPb (Figure 1).…”

Section: Cbp and P300mentioning

confidence: 99%

“…This type of bridging activity could explain the ability of Myb proteins to cooperate with C/EBPb and a wide variety of other transcription factors, in the context of di erent promoters. CBP and p300 bind the transactivation domains of c-Myb and C/EBPb, located in their central and N-terminal domains, respectively (Dai et al, 1996;Kietwitz and Wolfes, 1997;Mink et al, 1997;OelgeschlaÈ ger et al, 1996). This suggests that the coactivators are involved in mediating the transactivation activity of Myb and C/EBPb.…”

Section: Cbp and P300mentioning

confidence: 99%

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Myb binding proteins: regulators and cohorts in transformation

Ness

1999

Oncogene

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The c-Myb and v-Myb proteins are transcription factors that regulate cell proliferation and di erentiation. Both Myb proteins have been shown to interact with a number of cellular proteins, some of which are transcription factors that cooperate to activate speci®c promoters, while others regulate the transcriptional activity of Myb in speci®c contexts. By comparing and analysing the types of proteins that bind Myb, and the conserved domains of Myb that interact with other proteins, conclusions can be drawn regarding the role of speci®c partner proteins in the regulation of gene expression, cell proliferation and disease.

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Section: Cbp and P300mentioning

confidence: 99%

Section: Cbp and P300mentioning

confidence: 99%

Myb binding proteins: regulators and cohorts in transformation

Ness

1999

Oncogene

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“…The bcl-2 gene, which serves an antiapoptotic function in various cell types, has very recently been reported as a Myb target gene (Salomoni et al, 1997;Taylor et al, 1996;Frampton et al, 1996). Other transcription factors can cooperate with Myb to achieve maximal levels of transcriptional activation (Oelgeschlager et al, 1996;Dai et al, 1996;Hernandez-Munain and Krangel, 1995;Shapiro, 1995;McCracken et al, 1994;Burk et al, 1993;Ness et al, 1993), and thus may enhance transactivation of target genes and direct cellular speci®city.…”

Section: Introductionmentioning

confidence: 99%

Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2

et al. 1997

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Primary murine fetal hemopoietic cells were transformed with a fusion protein consisting of the ligand-binding domain of the estrogen receptor and a carboxylterminally truncated c-Myb protein (ERMYB). The ERMYB-transformed hemopoietic cells exhibit an immature myeloid phenotype when grown in the presence of b-estradiol. Upon removal of b-estradiol, the ERMYB cells display increased adherence, decreased clonogenicity and di erentiate to cells exhibiting granulocyte or macrophage morphology. The expression of the c-myc, ckit, cdc2 and bcl-2 genes, which are putatively regulated by Myb, was investigated in ERMYB cells grown in the presence or absence of b-estradiol. Neither c-myc nor cdc2 expression was down-regulated after removal of bestradiol demonstrating that di erentiation is not a consequence of decreased transactivation of these genes by ERMYB. While bcl-2 expression was reduced by 50% in ERMYB cells grown in the absence of bestradiol, there was no increase in DNA laddering, suggesting that Myb was not protecting ERMYB cells from apoptosis. In contrast, a substantial (200-fold) decrease in c-kit mRNA level was observed following di erentiation of ERMYB cells, and c-kit mRNA could be partially re-induced by the re-addition of b-estradiol. Furthermore, a reporter construct containing the c-kit promoter was activated when cotransfected with a Myb expression vector, providing further evidence of a role for Myb in the regulation of c-kit.

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“…CBP was originally reported as a coactivator of CREB (Chrivia et al, 1993;Kwok et al, 1994), however it turned out to be a multifunctional co-activator of various transcription factors, including c-Myb and GATA-1 (Blobel et al, 1998;Dai et al, 1996;Mink et al, 1997;Oelgeschlager et al, 1996). In this study, we reveal the inhibitory interaction of cMyb and GATA-1, which is probably mediated by CBP.…”

Section: Introductionmentioning

confidence: 58%

“…The Myb-VP16 and its reporter plasmid were described previously (Kanei Ishii et al, 1997). pGST-CBP265 (KIX, amino acids 460 ± 683) and pGST-c-Myb CTL were used to express various forms of GST-CBP and GSTMyb fusion proteins in E. coli (Dai et al, 1996;Nomura et al, 1993). pGST-C/H1 and pGST-GATA-1 were made by inserting the mouse CBP cDNA fragment (amino acids 287 ± 447) and the blunted NcoI fragment of GATA-1 cDNA into the SmaI site of the pGEX-2T (Pharmacia, Uppsala, Sweden) vector, respectively.…”

Section: Plasmidsmentioning

confidence: 99%

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

et al. 2000

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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.

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CBP as a transcriptional coactivator of c-Myb.

Cited by 337 publications

References 54 publications

Myb binding proteins: regulators and cohorts in transformation

Myb binding proteins: regulators and cohorts in transformation

Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2

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

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