Structure and biological activity of the transcriptional initiation sequences of the murine c-myb oncogene.
Structure and biological activity of the transcriptional initiation sequences of the murine c-myb oncogene.
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鼠 c-myb 癌基因转录起始序列的结构和生物活性。
DOI：
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发表时间：
1989
影响因子：
14.9
通讯作者：
Ashley R. Dunn
中科院分区：
文献类型：
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作者：
Peter W. Sobieszczuk;Thomas J. Gonda;Ashley R. Dunn
为了研究控制 c-myb 转录的控制机制，已分离出与鼠 c-myb 基因 5' 区域相对应的基因组克隆，并对其结构和功能进行了表征。引物延伸和核酸酶保护分析揭示了多个转录起始位点的存在，这些位点被用于多种造血细胞系（WEHI3B(D+)、FDC-P1 和 RB22.2）。一些位点用于所有细胞系，但其他位点是独特的；所有这些都位于 c-myb 基因的一个富含 G-C 的区域，包含许多潜在的 Sp1 结合位点，并且缺乏经典的启动子共有序列。进行了一些实验，其中控制报告基因表达的充分表征的启动子已被 c-myb DNA 片段（包括观察到的帽位点）取代，试图证明启动子在各种细胞类型中的活性。结果表明，c-myb 基因的一个区域（距离第一个外显子剪接供体位点上游约 1.0 kbp）包含一个弱启动子，该启动子在造血细胞和成纤维细胞中具有低水平的转录活性。这些结果支持这样的观点：c-myb 表达主要不是在转录起始水平上受到调节。
To study the control mechanism(s) that govern the transcription of c-myb, genomic clones corresponding to the 5' region of the murine c-myb gene have been isolated and characterized structurally and functionally. Primer extension and nuclease protection analysis have revealed the presence of multiple transcriptional initiation sites, that are utilized in several hemopoietic cell lines (WEHI3B(D+). FDC-P1 and RB22.2). Some of the sites are used in all cell lines but others are unique; all are located in a region of the c-myb gene that is G-C rich, contains a number of potential Sp1 binding sites and lacks classical promoter consensus sequences. Experiments in which well characterized promoters controlling expression of a reporter gene have been replaced by fragments of c-myb DNA (including the observed cap sites) were performed in an attempt to demonstrate promoter activity in various cell types. It was shown that a region of the c-myb gene (approximately 1.0 kbp upstream from the splice donor site of the first exon) contains a weak promoter that has a low level of transcriptional activity in hemopoietic as well as in fibroblastic cells. These results support the suggestion that c-myb expression is not regulated primarily at the level of initiation of transcription.