TRANS ACTIVATION OF GENE-EXPRESSION BY V-MYB
TRANS ACTIVATION OF GENE-EXPRESSION BY V-MYB
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DOI：
10.1128/mcb.10.5.2285
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发表时间：
1990-05-01
影响因子：
5.3
通讯作者：
LIPSICK, JS
中科院分区：
文献类型：
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作者：
IBANEZ, CE;LIPSICK, JS
v-myb致癌基因在鸡体内引起急性髓细胞白血病，并在体外转化禽髓细胞。它的产物p48v-myb是一种结合DNA的短命核蛋白。我们证明p48v-myb在瞬时DNA转染实验中可以作为基因表达的反式激活因子。反式激活需要高度保守的氨基端dna结合域和不太保守的p48v-myb的羧基端结合域，两者都是转化所必需的。插入单纯疱疹病毒胸苷激酶启动子上游的p48v-myb结合DNA的一致序列的多个拷贝强烈刺激v-myb-VP16融合蛋白的转录激活，但不刺激p48v-myb本身，这表明p48v-myb与DNA的结合可能不足以进行反式激活。
The v-myb oncogene causes acute myelomonocytic leukemia in chickens and transforms avian myeloid cells in vitro. Its product, p48v-myb, is a short-lived nuclear protein which binds DNA. We demonstrate that p48v-myb can function as a trans activator of gene expression in transient DNA transfection assays. trans activation requires the highly conserved amino-terminal DNA-binding domain and the less highly conserved carboxyl-terminal domain of p48v-myb both of which are required for transformation. Multiple copies of a consensus sequence for DNA binding by p48v-myb inserted upstream of a herpes simplex virus thymidine kinase promoter are strongly stimulatory for transcriptional activation by a v-myb-VP16 fusion protein but not by p48v-myb itself, suggesting that the binding of p48v-myb to DNA may not be sufficient for trans activation.