Glucocorticoid responsiveness of mouse mammary tumor virus (MMTV) promoters in a down-transcription hepatoma tissue culture (HTC) variant.
Glucocorticoid responsiveness of mouse mammary tumor virus (MMTV) promoters in a down-transcription hepatoma tissue culture (HTC) variant.
复制标题
下调转录肝癌组织培养（HTC）变体中小鼠乳腺肿瘤病毒（MMTV）启动子的糖皮质激素反应性。
DOI：
10.1016/0303-7207(89)90189-5
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发表时间：
1989
影响因子：
4.1
通讯作者：
Firestone,GL
中科院分区：
文献类型：
--
作者：
John,NJ;Bravo,DA;Firestone,GL
补体介导的细胞溶解小鼠乳腺肿瘤病毒（MMTV）感染的大鼠肝癌（HTC）细胞系，M1.54，导致恢复的突变衍生物，命名为CR5，其中基础和地塞米松诱导的前病毒MMTV RNA表达的幅度被选择性降低。用含有糖皮质激素调节的MMTV启动子连接到新霉素抗性基因（pLNL）的质粒转染变体CR5细胞。在pLNL转染的CR5和M1.54细胞中，对G418杀伤的半数最大抗性是糖皮质激素诱导的，并且依赖于糖皮质激素受体占有率。MMTV前病毒序列的下调不能被赋予由相同病毒启动子驱动的转染基因，这表明CR5细胞是有缺陷的切割因子。与这一观点一致，瞬时异核体的间接免疫荧光显示未感染的野生型HTC细胞未能补充CR5中的缺陷，而CR5细胞不抑制M1.54细胞的野生型表型。
Complement-mediated cytolysis of the mouse mammary tumor virus (MMTV)-infected rat hepatoma (HTC) cell line, M1.54, resulted in recovery of a mutant derivative, designated CR5, in which the magnitude of both basal and dexamethasone-induced proviral MMTV RNA expression was selectively reduced. Variant CR5 cells were transfected with a plasmid containing the glucocorticoid-regulated MMTV promotor linked to the neomycin resistance gene (pLNL). Half-maximal resistance to G418 killing was glucocorticoid inducible in both pLNL-transfected CR5 and M1.54 cells and was dependent on glucocorticoid receptor occupancy. The down-transcription of MMTV provirus sequences cannot be conferred to transfected genes driven by the same viral promoter suggesting that CR5 cells are defective incisacting factors. Consistent with this notion, indirect immunofluorescence of transient heterokaryons revealed that uninfected wild-type HTC cells failed to complement the defect in CR5 while CR5 cells did not suppress the wild-type phenotype of M1.54 cells.