Robey W G, Oskarsson M K, Vande Woude G F, Naso R B, Arlinghaus R B, Haapala D K, Fischinger P J
Cell. 1977 Jan;10(1):79-89. doi: 10.1016/0092-8674(77)90142-8.
It was previously demonstrated that the 60,000 dalton (p60) precursor-like polyprotein containing murine p30 was a constituent of the feline leukemia virus pseudotype of Moloney sarcoma virus [m1MSV(FeLV)]. It is now shown that p60 is detected in cells of five mammalian species transformed by m1MSV, indicating that p60 is specified by this genome. Moreover, little or no murine p30 is detected in the m1MSV-transformed cells, suggesting that the murine group p30 antigenic reactivity of S + L- cells is ude to p60. Pulse-chase studies in cells producing m1MSV(FeLV) show that p60 is the largest polypeptide detectable during the pulse, and that intracellular p60 is not cleaved into smaller (for example, p30) polypeptides during chase periods of up to 10 hr. The lack of cleavage of p60 is in contrast to the properties of p30 precursors detected in cells containing replicating avian or mammalian RNA tumor viruses. The inefficient cleavage of intracellular p60 and the kinetics of appearance of murine p30 in extracellular m1MSV(FeLV) suggest that p60 cleavage to p30 occurs in cells shortly before virus release. While only p60 was detected in the m1MSV-transformed cells, p60 and p70 were detected in m3MSV-transformed cells, and no immunoprecipitable polypeptides were detected in HT-1 MSV-transformed cells. The observed differences in the intracellular polypeptide expression by each of the strains of MSV suggests differences in genetic content.
先前已证明，含有鼠源p30的60,000道尔顿（p60）前体样多聚蛋白是莫洛尼肉瘤病毒猫白血病病毒假型[m1MSV(FeLV)]的一个组成部分。现在发现，在被m1MSV转化的五种哺乳动物细胞中检测到了p60，这表明p60是由该基因组所决定的。此外，在m1MSV转化的细胞中几乎检测不到或未检测到鼠源p30，这表明S + L-细胞的鼠源p30抗原反应性归因于p60。对产生m1MSV(FeLV)的细胞进行的脉冲追踪研究表明，p60是脉冲期间可检测到的最大多肽，并且在长达10小时的追踪期内，细胞内的p60不会裂解成更小的（例如p30）多肽。p60不发生裂解这一情况与在含有复制性禽或哺乳动物RNA肿瘤病毒的细胞中检测到的p30前体的特性形成对比。细胞内p60裂解效率低下以及鼠源p30在细胞外m1MSV(FeLV)中出现的动力学表明，p60裂解为p30发生在病毒释放前不久的细胞中。虽然在m1MSV转化的细胞中仅检测到p60，但在m3MSV转化的细胞中检测到了p60和p70，而在HT-1 MSV转化的细胞中未检测到可免疫沉淀的多肽。观察到的每种MSV毒株在细胞内多肽表达上的差异表明其遗传内容存在差异。
