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Effect of loss of thymidine kinase activity on the tumorigenicity of clones of SV40-transformed hamster cells.胸苷激酶活性丧失对SV40转化的仓鼠细胞克隆致瘤性的影响。
Proc Natl Acad Sci U S A. 1970 Oct;67(2):1042-9. doi: 10.1073/pnas.67.2.1042.
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Avian sarcoma virus transformed hamster cells resistant to bromodeoxyuridine and deficient in thymidine kinase activity.禽肉瘤病毒转化的仓鼠细胞对溴脱氧尿苷具有抗性且胸苷激酶活性不足。
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本文引用的文献

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INHIBITORS OF PROTEIN SYNTHESIS: EFFECT ON THE LEVELS OF DEOXYCYTIDYLATE DEAMINASE, THYMIDYLATE SYNTHETASE, AND THYMIDINE KINASE IN REGENERATING RAT LIVER.蛋白质合成抑制剂:对再生大鼠肝脏中脱氧胞苷酸脱氨酶、胸苷酸合成酶和胸苷激酶水平的影响
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2
STUDIES ON THYMIDINE KINASE IN CULTURED MOUSE FIBROBLASTS.培养的小鼠成纤维细胞中胸苷激酶的研究。
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SOME FACTORS AFFECTING THE PHOSPHORYLATION OF THYMIDINE BY TRANSPLANTABLE RAT HEPATOMAS.影响可移植大鼠肝癌细胞胸苷磷酸化的一些因素
Cancer Res. 1965 Apr;25:358-64.
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COCARCINOGENESIS.协同致癌作用
Br Med Bull. 1964 May;20:139-44. doi: 10.1093/oxfordjournals.bmb.a070307.
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VIRAL STUDIES OF SV40 TUMORIGENESIS IN HAMSTERS.仓鼠中SV40肿瘤发生的病毒学研究。
J Natl Cancer Inst. 1964 Jan;32:253-65.
6
AN ANALYSIS OF SV 40-INDUCED TRANSFORMATION OF HAMSTER KIDNEY TISSUE IN VITRO. II. STUDIES OF THREE CLONES DERIVED FROM A CONTINUOUS LINE OF TRANSFORMED CELLS.体外仓鼠肾组织的SV 40诱导转化分析。II. 源自连续转化细胞系的三个克隆的研究。
Proc Natl Acad Sci U S A. 1963 Nov;50(5):847-54. doi: 10.1073/pnas.50.5.847.
7
THE INOSINIC ACID PYROPHOSPHORYLASE ACTIVITY OF MOUSE FIBROBLASTS PARTIALLY RESISTANT TO 8-AZAGUANINE.对8-氮杂鸟嘌呤有部分抗性的小鼠成纤维细胞的肌苷酸焦磷酸化酶活性
Proc Natl Acad Sci U S A. 1963 Sep;50(3):568-73. doi: 10.1073/pnas.50.3.568.
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DELETION OF THYMIDINE KINASE ACTIVITY FROM L CELLS RESISTANT TO BROMODEOXYURIDINE.从对溴脱氧尿苷有抗性的L细胞中删除胸苷激酶活性。
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Induction of thymidine kinase by vaccinia-infected mouse fibroblasts.痘苗病毒感染的小鼠成纤维细胞诱导胸苷激酶的产生。
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Physiological thymidine reutilization in rat bone marrow.大鼠骨髓中生理状态下的胸苷再利用
Proc Soc Exp Biol Med. 1966 Jun;122(2):448-55. doi: 10.3181/00379727-122-31159.

胸苷激酶活性丧失对SV40转化的仓鼠细胞克隆致瘤性的影响。

Effect of loss of thymidine kinase activity on the tumorigenicity of clones of SV40-transformed hamster cells.

作者信息

Rothschild H, Black P H

出版信息

Proc Natl Acad Sci U S A. 1970 Oct;67(2):1042-9. doi: 10.1073/pnas.67.2.1042.

DOI:10.1073/pnas.67.2.1042
PMID:4331716
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC283310/
Abstract

Cells deficient in the enzyme thymidine kinase were derived from transplantable SV40-transformed hamster cells. The resultant cell lines were less transplantable when inoculated into hamsters. Tumors which did arise from such cells had prolonged latent periods and were found to contain a mixture of enzyme-containing and enzyme-deficient cells. Revertant cell lines obtained either spontaneously or after mutagenesis in vitro contained intermediate levels of thymidine kinase activity and displayed an oncogenic potential which was intermediate between the wild type and enzyme-deficient cells. It is postulated that salvage pathway enzymes may play a rate-limiting role in tumorigenesis.

摘要

缺乏胸苷激酶的细胞源自可移植的SV40转化仓鼠细胞。将所得细胞系接种到仓鼠体内时,其移植能力较低。由这类细胞产生的肿瘤潜伏期延长,且发现含有含酶细胞和缺酶细胞的混合物。自发获得或体外诱变后获得的回复细胞系含有中等水平的胸苷激酶活性,并表现出介于野生型细胞和缺酶细胞之间的致癌潜力。据推测,补救途径酶可能在肿瘤发生中起限速作用。