Zoidl G, Brockmann D, Esche H
Institute of Molecular Biology (Cancer Research), Medical School Essen, Germany.
Gene. 1993 Sep 15;131(2):269-74. doi: 10.1016/0378-1119(93)90305-m.
The protein product (c-Myc) of the human c-myc proto-oncogene carries a beta-turn/alpha-helix motif at the exon2/exon3 boundary. The amino acid (aa) sequence and secondary structure of this motif are highly conserved among several nuclearly localized oncogene products, c-Myc, N-Myc, c-Fos, SV40 large T and adenovirus (Ad) Ela. Removal of this region from Ad E1a results in the loss of the transforming properties of the virus without destroying its known transregulatory functions. In order to analyse whether deletion of the above-mentioned region from c-Myc has a similar effect on its transformation activity, we constructed a deletion mutant (c-myc delta) lacking the respective aa at the exon2/exon3 boundary. In contrast to the c-myc wild-type gene product, constitutive expression of c-myc delta does not lead to the immortalization of primary mouse embryo fibroblast cells (MEF cells). This result indicates that c-Myc and Ad El a share a common domain which is involved in the transformation process by both oncogenes.
人类原癌基因c-myc的蛋白质产物（c-Myc）在第2外显子/第3外显子边界处带有一个β-转角/α-螺旋基序。该基序的氨基酸（aa）序列和二级结构在几种核定位癌基因产物（c-Myc、N-Myc、c-Fos、SV40大T抗原和腺病毒（Ad）E1a）中高度保守。从Ad E1a中去除该区域会导致病毒失去转化特性，而不破坏其已知的反式调节功能。为了分析从c-Myc中删除上述区域是否对其转化活性有类似影响，我们构建了一个缺失突变体（c-myc delta），该突变体在第2外显子/第3外显子边界处缺失了相应的氨基酸。与c-myc野生型基因产物相反，c-myc delta的组成型表达不会导致原代小鼠胚胎成纤维细胞（MEF细胞）永生化。这一结果表明，c-Myc和Ad E1a共享一个共同结构域，该结构域参与了这两种癌基因的转化过程。
