Fig. 5.
Fig. 5. AML1-ETO down-regulates transactivation capacity of PU.1 in myeloid cells and the expression of the PU.1 target genes in AML patients with t(8;21). / (A) AML1-ETO down-regulates transactivation of PU.1 in myeloid cells. U937 cells were electroporated with wild-type M-CSF receptor promoter, M-CSF receptor promoter without (w/o) AML1-binding site, p(PU.1)4TK, p(mutPU.1)4TK, or pXP2 with and without AML1-ETO. (B) Low expression of PU.1 target genes in patients with t(8;21). AML patients (n = number of patients) with t(8;21) have fewer positive cells for cell surface markers regulated by PU.1 as compared to patients without t(8;21). CD14 and CD64 promoters have PU.1-binding sites, but no putative C/EPBα-, AML1-, or MEF-binding sites.

AML1-ETO down-regulates transactivation capacity of PU.1 in myeloid cells and the expression of the PU.1 target genes in AML patients with t(8;21).

(A) AML1-ETO down-regulates transactivation of PU.1 in myeloid cells. U937 cells were electroporated with wild-type M-CSF receptor promoter, M-CSF receptor promoter without (w/o) AML1-binding site, p(PU.1)4TK, p(mutPU.1)4TK, or pXP2 with and without AML1-ETO. (B) Low expression of PU.1 target genes in patients with t(8;21). AML patients (n = number of patients) with t(8;21) have fewer positive cells for cell surface markers regulated by PU.1 as compared to patients without t(8;21). CD14 and CD64 promoters have PU.1-binding sites, but no putative C/EPBα-, AML1-, or MEF-binding sites.

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