Vousden K H, Crook T, Farrell P J
Ludwig Institute for Cancer Research, St Mary's Hospital Medical School, London, U.K.
J Gen Virol. 1993 May;74 ( Pt 5):803-10. doi: 10.1099/0022-1317-74-5-803.
Wild-type human p53 and a series of p53 point mutants isolated from Burkitt's lymphoma (BL) cell lines were tested for their ability to inhibit DNA synthesis in a p53-negative BL cell line and to bind and be degraded by the human papillomavirus type 16 E6 protein. All the mutants lost the wild-type ability to inhibit DNA synthesis, demonstrating that they are all functionally altered. Binding to E6 and consequent degradation of the p53 mutants frequently correlated with changed suppressor properties in BL cells.
对野生型人p53以及从伯基特淋巴瘤(BL)细胞系中分离出的一系列p53点突变体进行了测试,以考察它们在一个p53阴性的BL细胞系中抑制DNA合成的能力,以及与人乳头瘤病毒16型E6蛋白结合和被其降解的能力。所有突变体均丧失了野生型抑制DNA合成的能力,表明它们在功能上均发生了改变。p53突变体与E6的结合以及随之而来的降解,常常与BL细胞中抑制特性的改变相关。