Jochemsen A G, de Wit C M, Bos J L, van der Eb A J
Virology. 1986 Jul 30;152(2):375-83. doi: 10.1016/0042-6822(86)90140-6.
A mutant Ad12 E1A region (Ad12 R11E1A) was constructed, which directs the synthesis of only a 15-kDa N-terminal E1A product. When controlled by the SV40 early promoter plus enhancer region (SVR11E1A) this mutant E1A region is capable of immortalizing primary baby rat kidney (BRK) cells, showing that the information essential for immortalization is located in the N-terminal part of region E1A and is shared by the 13 S and 12 S mRNA gene products. This immortalization is thought to be an essential step in the process of oncogenic transformation. Primary BRK cells transformed by SVR11E1A in the presence of Ad12 E1B are nononcogenic. This implies that the E1A region also codes for activities required for oncogenicity. However, in the presence of an activated c-Ha-ras oncogene the SVR11E1A region can oncogenically transform primary BRK cells, showing that the c-Ha-ras oncogene not only can complement for the Ad12 E1B region, but also for the E1A function lost by the R11 deletion.
构建了一种突变型腺病毒12型E1A区（Ad12 R11E1A），其仅指导合成一种15 kDa的N端E1A产物。当由猴病毒40早期启动子加增强子区域（SVR11E1A）控制时，该突变型E1A区能够使原代新生大鼠肾（BRK）细胞永生化，表明永生化所必需的信息位于E1A区的N端部分，并且由13 S和12 S mRNA基因产物共享。这种永生化被认为是致癌转化过程中的一个关键步骤。在腺病毒12型E1B存在的情况下，由SVR11E1A转化的原代BRK细胞不具有致癌性。这意味着E1A区也编码致癌所需的活性。然而，在存在激活的c-Ha-ras癌基因的情况下，SVR11E1A区可以致癌性地转化原代BRK细胞，表明c-Ha-ras癌基因不仅可以补充腺病毒12型E1B区，还可以补充因R11缺失而丧失的E1A功能。
