Dudek H, Reddy E P
Wistar Institute, Philadelphia, Pennsylvania 19104.
Oncogene. 1989 Dec;4(12):1489-95.
Using a panel of anti-myb antibodies, we have examined the c-myb proteins present in the NFS-60 and ABPL-1, ABPL-2, and ABPL-4 tumor cell lines, all of which have an altered myb locus due to viral insertional mutagenesis. As predicted from previous DNA and RNA analysis, NFS-60 cells produce myb protein with a truncated C-terminus and a normal N-terminus. The three ABPL tumor cell lines studied here were previously shown to have undergone similar rearrangements towards the 5' end of myb locus and were expected to synthesize identical myb RNAs and proteins. These cell lines were found to produce myb proteins with N-terminal modifications. Surprisingly, however, the three cell lines were found to synthesize a heterogenous array of myb proteins of different sizes. These observations suggest that oncogenic activation of myb in ABPL tumors may involve additional changes in the coding region in addition to those occurring at the N-terminus.
我们使用一组抗myb抗体，检测了NFS - 60和ABPL - 1、ABPL - 2及ABPL - 4肿瘤细胞系中存在的c - myb蛋白，所有这些细胞系由于病毒插入诱变而具有改变的myb基因座。正如先前DNA和RNA分析所预测的，NFS - 60细胞产生具有截短C末端和正常N末端的myb蛋白。这里研究的三个ABPL肿瘤细胞系先前已显示在myb基因座的5'端发生了类似的重排，预计会合成相同的myb RNA和蛋白质。发现这些细胞系产生具有N末端修饰的myb蛋白。然而，令人惊讶的是，发现这三个细胞系合成了一系列大小不同的异源myb蛋白。这些观察结果表明，ABPL肿瘤中myb的致癌激活可能除了在N末端发生的变化外，还涉及编码区的其他变化。
