Transcriptional activation by the v-myb oncogene and its cellular progenitor, c-myb.
Transcriptional activation by the v-myb oncogene and its cellular progenitor, c-myb.
复制标题
DOI：
10.1016/0168-9525(89)90128-5
复制
发表时间：
1989
期刊：
影响因子：
64.5
通讯作者：
Kathleen Weston;J.Michael Bishop
中科院分区：
文献类型：
--
作者：
Kathleen Weston;J.Michael Bishop
V-myb癌基因，就像它的细胞前体c-myb一样，编码一种短暂的核蛋白，参与影响多种细胞类型的生长和分化的过程。融合蛋白中的v-MYB序列连接到酵母转录激活因子GAL4的DNA结合域，可以激活从顺式连接的报告基因到GAL4结合位点的转录。负责转录激活的v-myb结构域位于残基204和254之间，是激活的必要条件和充分条件。完整的v-myb和c-myb蛋白也可以通过顺式连接到报告基因的myb结合位点来激活转录。在激活域缺失的v-myb蛋白不再能够刺激转录。
The v-myb oncogene, like its cellular progenitor c-myb, encodes a short-lived nuclear protein involved in processes affecting growth and differentiation in a number of cell types. Fusion proteins, in which v-myb sequences are linked to the DNA binding domain of the yeast transcriptional activator GAL4, can activate transcription from a reporter gene linked in cis to a GAL4 binding site. The domain of v-myb responsible for transcriptional activation is located between residues 204 and 254, and is both necessary and sufficient for activation. Intact v-myb and c-myb proteins can also activate transcription, via a myb binding site linked in cis to a reporter gene. A v-myb protein bearing a deletion in the activator domain is no longer capable of stimulating transcription.