Daley G Q, McLaughlin J, Witte O N, Baltimore D
Science. 1987 Jul 31;237(4814):532-5. doi: 10.1126/science.2440107.
The v-abl oncogene of the Abelson murine leukemia virus (A-MuLV) is known to efficiently transform NIH/3T3 fibroblasts in vitro and to cause an acute lymphosarcoma in susceptible murine hosts. The role of its relative, the bcr/abl gene product, in the etiology of human chronic myelogenous leukemia (CML) remains speculative. To assess the transforming properties of the bcr/abl gene product, complementary DNA clones encoding the CML-specific P210 bcr/abl protein were expressed in NIH/3T3 fibroblasts. In contrast to the v-abl oncogene product P160, the P210 bcr/abl gene product did not transform NIH/3T3 cells. Cell lines were isolated that expressed high levels of the P210 bcr/abl protein but were morphologically normal. During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein. This suggests that a property of viral gag sequences, probably myristylation-dependent membrane localization, must be provided to bcr/abl for it to transform fibroblasts.
阿贝尔森鼠白血病病毒（A-MuLV）的v-abl癌基因已知能在体外有效转化NIH/3T3成纤维细胞，并在易感鼠宿主中引发急性淋巴肉瘤。其相关基因bcr/abl的基因产物在人类慢性粒细胞白血病（CML）病因学中的作用仍属推测。为评估bcr/abl基因产物的转化特性，编码CML特异性P210 bcr/abl蛋白的互补DNA克隆在NIH/3T3成纤维细胞中表达。与v-abl癌基因产物P160不同，P210 bcr/abl基因产物并未转化NIH/3T3细胞。分离出了表达高水平P210 bcr/abl蛋白但形态正常的细胞系。在这些实验过程中，分离出了一种bcr/abl的转化重组体，它将来自辅助病毒的gag决定簇融合到bcr/abl蛋白的氨基末端。这表明，必须为bcr/abl提供病毒gag序列的一种特性，可能是肉豆蔻酰化依赖性膜定位，才能使其转化成纤维细胞。
