Ibanez C E, Lipsick J S
Department of Pathology, University of California, San Diego School of Medicine, La Jolla 92093.
Mol Cell Biol. 1990 May;10(5):2285-93. doi: 10.1128/mcb.10.5.2285-2293.1990.
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.
v-myb致癌基因可引发鸡的急性髓单核细胞白血病,并在体外使禽类髓细胞发生转化。其产物p48v-myb是一种与DNA结合的寿命短暂的核蛋白。我们证明,在瞬时DNA转染试验中,p48v-myb可作为基因表达的反式激活因子发挥作用。反式激活需要p48v-myb高度保守的氨基末端DNA结合结构域和保守性稍低的羧基末端结构域,这两个结构域对于转化都是必需的。插入单纯疱疹病毒胸苷激酶启动子上游的、p48v-myb结合DNA的共有序列的多个拷贝,对v-myb-VP16融合蛋白介导的转录激活有强烈的刺激作用,但对p48v-myb本身介导的转录激活却无此作用,这表明p48v-myb与DNA的结合可能不足以实现反式激活。