Kit S
Mol Cell Biochem. 1976 Jun 15;11(3):161-82. doi: 10.1007/BF01744997.
A resume has been presented of some recent investigations which show that DNA synthesis can be initiated in many types of quiescent animal cells by external stimuli, by introducing a quiescent nucleus into the cytoplasm of a proliferating cell, or by a virus infection. The components of the DNA replication apparatus are described. It is shown that deoxyribonucleoside triphosphate pools increase substantially in animal cells at the time DNA synthesis is initiated due to the enhanced activities of enzymes functioning in nucleotide synthesis. Especially striking is the increase of thymidine kinase activity, indicating that this enzyme may be a useful marker of the shift from the quiescent to the replicative state. The thymidine kinase isozymes of vertebrate cells have been characterized. Thymidine kinase F, which is found principally in the cytosol, is the isozyme that increases when G1 (Go) phase cells are stimulated or infected with oncogenic viruses. Chick cytosol thymidine kinase F can also be reactivated by introducing differentiated chick erythrocyte nuclei into the cytoplasm of enzyme-deficient LM (TK-) mouse cells. Furthermore, herpesviruses code for distinctive, virus-specific thymidine kinase isozymes, so that another way to transform thymidine kinase-deficient LM TK-) cells to kinase-positive cells is by infecting them with UV-irradiated herpes simplex viruses. The experiments on the activation of DNA synthesis and thymidine kinase F activity have been discussed in the context of the proliferative activity in vivo and the immortalization in culture of neoplastic cells. These experiments suggest that genes determining cell cycle proteins are readily accessible to transcription and translation in essentially all nucleated cells. The tendency of transformed cells to become multinucleated after cytochaliasin B treatment also suggests that one important difference between malignant cells and most normal cells may be the ability of malignant cells to 'stockpile' the proteins (and/or their messenger RNAs) of the DNA replicative apparatus and to maintain the 'stockpiles' in progeny cells.
本文综述了一些近期的研究，这些研究表明，在多种静止的动物细胞中，DNA合成可通过外部刺激、将静止细胞核导入增殖细胞的细胞质或病毒感染来启动。文中描述了DNA复制装置的组成成分。结果显示，在DNA合成启动时，动物细胞中的脱氧核糖核苷三磷酸池会大幅增加，这是由于核苷酸合成中发挥作用的酶活性增强所致。特别显著的是胸苷激酶活性的增加，这表明该酶可能是从静止状态转变为复制状态的一个有用标志物。已对脊椎动物细胞的胸苷激酶同工酶进行了表征。主要存在于胞质溶胶中的胸苷激酶F是当G1（G0）期细胞受到刺激或感染致癌病毒时增加的同工酶。将分化的鸡红细胞核导入缺乏该酶的LM（TK-）小鼠细胞的细胞质中，也可使鸡胞质溶胶胸苷激酶F重新激活。此外，疱疹病毒编码独特的、病毒特异性的胸苷激酶同工酶，因此将胸苷激酶缺陷的LM（TK-）细胞转化为激酶阳性细胞的另一种方法是用紫外线照射的单纯疱疹病毒感染它们。已在体内增殖活性和肿瘤细胞培养永生化的背景下讨论了DNA合成激活和胸苷激酶F活性的实验。这些实验表明，决定细胞周期蛋白的基因在基本上所有有核细胞中都易于进行转录和翻译。用细胞松弛素B处理后转化细胞趋向于形成多核的趋势也表明，恶性细胞与大多数正常细胞之间的一个重要差异可能在于恶性细胞有能力“储存”DNA复制装置的蛋白质（和/或其信使RNA），并在子代细胞中维持这些“储存”。
