A dominant interfering Myb mutant causes apoptosis in T cells.

Taylor, Derek J.; Badiani, Pratipa; Weston, Kathleen

doi:10.1101/gad.10.21.2732

Cited by 179 publications

(172 citation statements)

References 51 publications

(62 reference statements)

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“…The regulation of apoptosis and bcl-2 expression by Myb has recently been reported (Salomoni et al, 1997;Taylor et al, 1996;Frampton et al, 1996). We show a continuing loss of viability and increased apoptosis in ERMYB cells when deprived of GM-CSF.…”

Section: Apoptosis In Ermyb Cellssupporting

confidence: 68%

“…Myb up-regulates bcl-2 and suppresses apoptosis in at least some myeloid and T cells (Salomoni et al, 1997;Taylor et al, 1996;Frampton et al, 1996). To establish whether ERMYB cells were undergoing apoptosis upon inactivation of Myb, the viability of ERMYB cells was examined following b-estradiol withdrawal.…”

Section: Apoptosis In Ermyb Cellsmentioning

confidence: 99%

“…Activation by Myb of T-lymphocyte speci®c genes such as CD4, T cell receptor d and lck tyrosine kinase and of genes which function in cell growth control such as cdc2 and c-myc has also been demonstrated (Hernandez-Munain and Krangel, 1995;McCracken et al, 1994;Cogswell et al, 1993;Ku et al, 1993;Siu et al, 1992;Nakagoshi et al, 1992;Evans et al, 1990). 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%

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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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Section: Apoptosis In Ermyb Cellssupporting

confidence: 68%

Section: Apoptosis In Ermyb Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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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“…Most importantly, the anti-myb sFvs inhibited the transactivation activity of Myb and this appeared to correlate with the cytotoxic e ect of the sFv in a Myb positive leukemia cell line, K562. The therapeutic utility of this interesting approach, and that of delivering dominant negative Myb constructs into hematopoietic cells (Taylor et al, 1996) remains to be tested. Alternative approaches include the use of triple helix forming oligodeoxynucleotides (Gunther et al, 1996), antisense oligodeoxynucleotides (ODN) , and ribozymes (Eckstein, 1996;James and Turner, 1997;Sullenger, 1995).…”

Section: Methodologic Considerationsmentioning

confidence: 99%

Myb targeted therapeutics for the treatment of human malignancies

Gewirtz

1999

Oncogene

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“…Intriguingly, the long period of latency, followed by the development of acute lymphoma, is very reminiscent of lymphomas induced by dysregulation of the bcl-2 oncogene (Linette et al, 1995). Loss of Myb activity in T cells has been shown to lead to an increased susceptibility to apoptosis (Taylor et al, 1996), and so it is possible that v-Myb and bcl-2 both cause lymphomas by prolonging the lifetime of a pool of cells, and thereby increasing the chance of further somatic mutations leading to tumor formation.…”

mentioning

confidence: 99%