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c-myb而非c-myc抑制小鼠红白血病细胞中血红素诱导的血红蛋白非终末表达。

c-myb but not c-myc suppresses the hemin-induced nonterminal expression of hemoglobin by murine erythroleukemia cells.

作者信息

Prochownik E V

机构信息

University of Michigan, Ann Arbor 48109.

出版信息

Blood. 1989 Feb 15;73(3):782-6.

PMID:2644989
Abstract

Clonal lines of Friend murine erythroleukemia (F-MEL) cells have been generated following transfection with c-myc or c-myb expression plasmids. These clones produce high levels of abnormally regulated proto-oncogene transcripts and fail to terminally differentiate in the presence of dimethyl sulfoxide. To determine the relative levels at which the two proto-oncogenes might exert their inhibitory effects, we asked whether these clones could express differentiated functions in the absence of terminal differentiation. It was found that exposure of c-myc-transfected cells to hemin allows for the induction of hemoglobin, whereas c-myb-transfected cells were refractory to hemin induction. It thus appears that c-myb exerts a more globally suppressive effect on F-MEL-differentiated functions than does c-myc and may prevent the expression of those events that can otherwise be dissociated from the terminally differentiated state.

摘要

用c-myc或c-myb表达质粒转染后,已产生了弗瑞德小鼠红白血病(F-MEL)细胞的克隆系。这些克隆产生高水平的异常调控的原癌基因转录本,并且在二甲基亚砜存在的情况下不能终末分化。为了确定这两个原癌基因发挥其抑制作用的相对水平,我们询问这些克隆在没有终末分化的情况下是否能够表达分化功能。结果发现,将转染了c-myc的细胞暴露于血红素可诱导血红蛋白的产生,而转染了c-myb的细胞对血红素诱导具有抗性。因此,似乎c-myb对F-MEL分化功能的抑制作用比c-myc更具全局性,并且可能阻止那些否则可以与终末分化状态分离的事件的表达。

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