Engelke U, Whittaker L, Lipsick J S
Department of Pathology, Stanford University School of Medicine, California 94305-5324, USA.
Virology. 1995 Apr 20;208(2):467-77. doi: 10.1006/viro.1995.1177.
The v-myb oncogene causes monoblastic leukemia in chickens and transforms avian myelomonocytic cells in vitro, v-Myb is a short-lived nuclear protein which binds to DNA in a sequence-specific manner and can activate gene expression in transient DNA transfections. Analysis of a series of v-Myb mutants has shown that the ability to activate transcription appears to be required for leukemic transformation. We have systematically investigated transcriptional activation by v-Myb and have made several new observations: (i) v-Myb is a very weak activator when compared to GAL4; (ii) very weak transcriptional activation by v-Myb is sufficient for transformation, whereas very strong transcriptional activation by a v-Myb-VP16 fusion protein is not; and (iii) v-Myb can activate transcription by two genetically distinct mechanisms, only one of which requires the presence of Myb-binding sites.
v-myb癌基因可引发鸡的单核细胞白血病,并在体外转化禽骨髓单核细胞。v-Myb是一种半衰期较短的核蛋白,它以序列特异性方式与DNA结合,并能在瞬时DNA转染中激活基因表达。对一系列v-Myb突变体的分析表明,激活转录的能力似乎是白血病转化所必需的。我们系统地研究了v-Myb的转录激活作用,并得出了一些新的观察结果:(i)与GAL4相比,v-Myb是一种非常弱的激活剂;(ii)v-Myb非常弱的转录激活作用就足以实现转化,而v-Myb-VP16融合蛋白非常强的转录激活作用则不然;(iii)v-Myb可通过两种遗传上不同的机制激活转录,其中只有一种机制需要Myb结合位点的存在。