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Thymidine Kinase from Normal Simian Virus 40-Transformed and Simian Virus 40-Lytically Infected Cells

机译:来自正常四面病毒40转化和四面病毒40淋巴液感染细胞的胸苷激酶

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摘要

Simian virus 40 (SV40) infection of human diploid cells failed to cause an enhanced production of thymidine kinase during the first 10 days after infection. Thymidine kinase activities from extracts of SV40-transformed cultures (human or simian) were considerably higher than the activity levels in extracts from the normal cells of origin. In addition, whereas the kinase activities obtained for human diploid cultures decreased as the cell sheet became confluent, the kinase activities for SV40-transformed human cells remained high after confluence was reached. Antisera obtained from hamsters bearing SV40 or adeno-7-SV40 hybrid virus tumors selectively inhibited enzyme from transformed sources (human or simian). Also, the antisera selectively inhibited enzyme extracted from SV40-lytically infected monkey cells. Sera from normal animals or from hamsters bearing polyoma tumors failed to inhibit enzymes from normal, SV40-transformed, or SV40-lytically infected cells. The Michaelis constant of partially purified enzyme from SV40-transformed cells was two to five times as high as that obtained for partially purified enzyme from human diploid cell cultures.
机译:人二倍体细胞的猿猴病毒40(SV40)感染在感染后的前10天内未能引起胸苷激酶的产生增加。 SV40转化培养物(人或猿猴)提取物中的胸苷激酶活性大大高于正常来源细胞提取物中的胸苷激酶活性。另外,尽管人类二倍体培养物获得的激酶活性随细胞片汇合而降低,但达到汇合后,SV40转化的人细胞的激酶活性仍然很高。从带有SV40或腺病毒7-SV40杂种病毒的仓鼠获得的抗血清选择性抑制转化来源(人或猿猴)的酶。同样,抗血清选择性抑制从SV40裂解感染的猴细胞中提取的酶。正常动物或携带多瘤瘤的仓鼠的血清不能抑制来自正常,SV40转化或SV40裂解感染细胞的酶。 SV40转化细胞中部分纯化的酶的米氏常数是人二倍体细胞培养物中部分纯化的酶的米氏常数的2至5倍。

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