Rowe D T, Graham F L
J Virol. 1983 Jun;46(3):1039-44. doi: 10.1128/JVI.46.3.1039-1044.1983.
Complementation group II host range mutants of adenovirus type 5 which map in early region 1B (E1B, 4.5 to 11.0 map units) have been shown to be defective for the synthesis of the E1B 58,000-dalton (58K) antigen in infections of HeLa or KB cells (Lassam et al., Cell 18:781-791, 1979) and unable to transform cultured rodent cells (Graham et al., Virology 86:10-21, 1978). In this report we show that DNA extracted from group II mutants hr6 and hr50 can transform rat cells with the same efficiency as wild-type DNA. Furthermore, group II mutant-transformed hamster cells were shown to contain no detectable E1B 58K tumor antigen but were capable of inducing tumors in newborn hamsters. Hamster cell lines 1019-3 and 1019-C3, transformed by hr50 DNA, produced no detectable quantities of either the E1B 58K or 19K antigen but nonetheless exhibited a fully transformed oncogenic phenotype. Our results show that the E1B 58K antigen is not absolutely required for oncogenic transformation and suggest that even cells lacking the 19K protein can be oncogenic.
已证明,腺病毒5型的互补群II宿主范围突变体定位于早期区域1B(E1B,4.5至11.0图距单位),在感染HeLa或KB细胞时,其合成E1B 58,000道尔顿(58K)抗原存在缺陷(拉萨姆等人,《细胞》18:781 - 791,1979年),并且无法转化培养的啮齿动物细胞(格雷厄姆等人,《病毒学》86:10 - 21,1978年)。在本报告中,我们表明,从II组突变体hr6和hr50中提取 的DNA能够以与野生型DNA相同的效率转化大鼠细胞。此外,II组突变体转化的仓鼠细胞未检测到E1B 58K肿瘤抗原,但能够在新生仓鼠中诱发肿瘤。由hr50 DNA转化的仓鼠细胞系1019 - 3和1019 - C3,未检测到E1B 58K或19K抗原,但仍表现出完全转化的致癌表型。我们的结果表明,致癌转化并不绝对需要E1B 58K抗原,并表明即使缺乏19K蛋白的细胞也可能具有致癌性。