Dobbelstein M, Arthur A K, Dehde S, van Zee K, Dickmanns A, Fanning E
Institute for Biochemistry, Munich, Germany.
Oncogene. 1992 May;7(5):837-47.
The ability of the oncogene products of DNA tumor viruses to induce DNA synthesis in quiescent cells is thought to depend on their capacity to bind to cellular proteins such as the retinoblastoma-suppressor protein Rb and the tumor suppressor p53, thereby abolishing the growth-arresting properties of these proteins. We have tested this hypothesis using SV40 T antigens carrying lesions that affect Rb binding, p53 binding or other functions involved in cell transformation. The results demonstrate that Rb binding is not essential for growth stimulation by T antigen. However, detailed analysis, including intracistronic complementation, suggests that at least three functions, Rb binding, a novel second activity localized to the DNA-binding domain and a function residing in the carboxy terminus, probably p53 binding, cooperate to generate the full growth induction potential of T antigen.
DNA肿瘤病毒的癌基因产物在静止细胞中诱导DNA合成的能力被认为取决于它们与细胞蛋白（如视网膜母细胞瘤抑制蛋白Rb和肿瘤抑制蛋白p53）结合的能力，从而消除这些蛋白的生长抑制特性。我们使用携带影响Rb结合、p53结合或参与细胞转化的其他功能的损伤的SV40 T抗原测试了这一假设。结果表明，Rb结合对于T抗原刺激生长并非必不可少。然而，包括顺反子内互补在内的详细分析表明，至少三种功能，即Rb结合、定位于DNA结合结构域的一种新的第二种活性以及存在于羧基末端的一种功能（可能是p53结合），共同发挥作用以产生T抗原的完全生长诱导潜能。
