Bos T J, Monteclaro F S, Mitsunobu F, Ball A R, Chang C H, Nishimura T, Vogt P K
Department of Microbiology, University of Southern California, School of Medicine, Los Angeles 90033.
Genes Dev. 1990 Oct;4(10):1677-87. doi: 10.1101/gad.4.10.1677.
To assess the transforming capability of the c-Jun protein, we introduced the chicken c-jun proto-oncogene into a replication competent avian retroviral expression vector (RCAS). Viral Jun efficiently transformed chicken embryo fibroblasts (CEFs) when expressed from this vector. Overexpression of c-Jun leads to transformation of CEFs with an efficiency that is 15- to 25-fold less than that seen for v-Jun, suggesting that v-Jun contains structural features that increase its oncogenic potential relative to c-Jun. There are four structural differences between v-Jun and c-Jun. To determine the relative contribution that each of these structural differences between v-Jun and c-Jun has on oncogenic activity, several deletion and substitution mutants were constructed. Each of these mutants was expressed in CEF and assayed for transformation by focus formation. Analysis of the results reveals that deletion of a region of 27 amino acids near the amino terminus of c-Jun and deletion of 3'-untranslated sequences are critical in activating the full oncogenic potential of Jun.
为了评估c-Jun蛋白的转化能力，我们将鸡c-jun原癌基因导入具有复制能力的禽逆转录病毒表达载体（RCAS）中。当从该载体表达时，病毒Jun能有效地转化鸡胚成纤维细胞（CEF）。c-Jun的过表达导致CEF转化，其效率比v-Jun低15至25倍，这表明v-Jun含有相对于c-Jun增加其致癌潜力的结构特征。v-Jun和c-Jun之间存在四个结构差异。为了确定v-Jun和c-Jun之间这些结构差异中的每一个对致癌活性的相对贡献，构建了几个缺失和替代突变体。这些突变体中的每一个都在CEF中表达，并通过集落形成法检测其转化情况。结果分析表明，c-Jun氨基末端附近27个氨基酸区域的缺失和3'非翻译序列的缺失对于激活Jun的全部致癌潜力至关重要。
