Inhibition of apoptosis by overexpressing Bcl-2 enhances gene amplification by a mechanism independent of aphidicolin pretreatment

Dong X. Yin; Robert T. Schimke

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Inhibition of apoptosis by overexpressing Bcl-2 enhances gene amplification by a mechanism independent of aphidicolin pretreatment

机译：通过过表达Bcl-2抑制凋亡可通过独立于蚜虫素预处理的机制增强基因扩增

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To study the effect of apoptosis on gene amplification, we have constructed HeLa S3 cell lines in which the expression of bcl-2 (BCL2) can be controlled by tetracy- cline in the growth medium. Induction of Bcl-2 expression caused a temporary delay of apoptosis and resulted in roughly a 3-fold increase in the frequency of resistant colonies when cells were selected with trimetrexate. This resistance was due to amplification of the dihydrofolate reductase gene.

机译：为了研究细胞凋亡对基因扩增的影响，我们构建了HeLa S3细胞系，其中bcl-2（BCL2）的表达可被四环素在生长培养基中控制。 Bcl-2表达的诱导导致细胞凋亡的暂时延迟，并且当使用曲美曲酯选择细胞时，导致耐药菌落的频率大约增加了3倍。该抗性归因于二氢叶酸还原酶基因的扩增。

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《Proceedings of the National Academy of Sciences of the United States of America》 |1996年第8期|p.3394-3398|共5页
作者
Dong X. Yin; Robert T. Schimke;
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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类自然科学总论;
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1. Dual inhibition of Bcl-2 and Bcl-xL Strikingly Enhances PI3K inhibition-induced apoptosis in human myeloid leukemia cells through a GSK3- and bim-dependent mechanism [J] . RahmaniM., AustM.M., AttkissonE., Cancer research: The official organ of the American Association for Cancer Research, Inc . 2013,第4期

机译：Bcl-2和Bcl-xL的双重抑制作用通过GSK3和Bim依赖性机制显着增强PI3K抑制诱导的人骨髓白血病细胞凋亡
2. The zebrafish bcl-2 homologue Nrz controls development during somitogenesis and gastrulation via apoptosis-dependent and -independent mechanisms. [J] . Arnaud E, Ferri KF, Thibaut J, Cell death and differentiation . 2006,第7期

机译：斑马鱼bcl-2同源物Nrz通过细胞凋亡依赖性和非依赖性机制控制着体发育和胃胚形成过程。
3. Suppression of apoptosis by Bcl-2 to enhance benzene metabolites-induced oxidative DNA damage and mutagenesis: A possible mechanism of carcinogenesis. [J] . Kuo ML, Shiah SG, Wang CJ, Molecular pharmacology. . 1999,第5期

机译：Bcl-2抑制细胞凋亡以增强苯代谢物诱导的氧化DNA损伤和诱变：致癌的可能机制。
4. Cathepsin D Overexpressed by Cancer Cells Can Enhance Apoptosis-dependent Chemo-sensitivity Independently of Its Catalytic Activity [C] . Melanie Beaujouin, Emmanuelle Liaudet-Coopma International Symposium on Hormonal Carcinogenesis . 2008

机译：癌症细胞过表达的组织蛋白酶D可以独立于其催化活性提高凋亡依赖性化学敏感性
5. Regulation of death receptor-mediated apoptosis by Bcl-2 and caspase inhibition. [D] . Johnson, Bryan Walter. 2002

机译：Bcl-2和caspase抑制调节死亡受体介导的细胞凋亡。
6. Inhibition of apoptosis by overexpressing Bcl-2 enhances gene amplification by a mechanism independent of aphidicolin pretreatment. [O] . D X Yin, R T Schimke 1996

机译：通过过度表达Bcl-2抑制凋亡可通过独立于蚜虫素预处理的机制增强基因扩增。
7. Inhibition of apoptosis by overexpressing Bcl-2 enhances gene amplification by a mechanism independent of aphidicolin pretreatment. [O] . Yin, D X, Schimke, R T 1996

机译：通过过度表达Bcl-2抑制凋亡可通过独立于蚜虫素预处理的机制增强基因扩增。

Inhibition of apoptosis by overexpressing Bcl-2 enhances gene amplification by a mechanism independent of aphidicolin pretreatment

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