A transactivator of c-myc is coordinately regulated with the proto-oncogene during cellular growth.
A transactivator of c-myc is coordinately regulated with the proto-oncogene during cellular growth.
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发表时间：
1995-06
期刊：
影响因子：
8
通讯作者：
L. Bazar;V. Harris;I. Sunitha;D. Hartmann;M. Avigan
中科院分区：
文献类型：
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作者：
L. Bazar;V. Harris;I. Sunitha;D. Hartmann;M. Avigan
最近克隆的一种核蛋白结合了人类c-myc原癌基因的远上游元件（FUSE），在未分化细胞中刺激启动子驱动的表达。随着c-myc表达的丧失，在pma诱导分化后的HL60细胞中，由于核径流测量的转录速率下降，FUSE结合蛋白（FBP） mRNA和蛋白水平都消失了。在这些细胞分化过程中，FBP mRNA的短暂半衰期（3小时）和蛋白的短暂半衰期（1.5小时）没有变化，通过免疫组织化学染色检测到核蛋白水平的快速下调。与c-myc一样，FBP在各种谱系的增殖细胞中表达，但在静止细胞中不表达。当T细胞和成纤维细胞被刺激从G0过渡到细胞周期时，FBP mRNA和DNA序列特异性核FBP结合活性都急剧上升，这与c-myc mRNA的出现有关。与许多其他直接早期生长反应基因的短暂表达不同，FBP和c-myc的表达都持续了24小时以上。在成纤维细胞中，FBP和c-myc在细胞周期的所有阶段的协调表达与FBP作为c-myc表达的生长依赖性调节剂的作用是一致的。
A recently cloned nuclear protein, which binds a far upstream element (FUSE) of the human c-myc proto-oncogene, stimulates promoter driven expression in undifferentiated cells. In concert with a loss of c-myc expression, both FUSE binding protein (FBP) mRNA and protein levels disappeared in HL60 cells after PMA-induced differentiation, due to a drop in the rate of transcription that was measured by nuclear runoff. During the differentiation of these cells, the brief half-lives of FBP mRNA (3 h) and protein (1.5 h) did not change, allowing for the rapid down-regulation of nuclear protein levels, as detected by immunohistochemical staining. Like c-myc, FBP is expressed in proliferating cells from a variety of lineages, but not in quiescent cells. When T cells and fibroblasts were stimulated to transit from G0 into the cell cycle, there was a dramatic rise of both FBP mRNA and DNA sequence specific nuclear FBP binding activity, which correlated with the appearance of c-myc mRNA. In contrast to the transient expression of many other immediate early growth response genes, both FBP and c-myc expression were sustained for more than 24 h. In fibroblasts, the coordinate expression of FBP and c-myc throughout all phases of the cell cycle is consistent with FBP's role as a growth-dependent regulator of c-myc expression.