Modeling the chemoprotective functions of glutathione S-transferases in cultured cell lines by heterologous expression.
Modeling the chemoprotective functions of glutathione S-transferases in cultured cell lines by heterologous expression.
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通过异源表达模拟培养细胞系中谷胱甘肽 S-转移酶的化学保护功能。
DOI：
10.1081/dmr-100101907
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Morrow,CS
中科院分区：
文献类型：
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作者：
Townsend,AJ;Fields,WR;Doss,AJ;Clapper,ML;Doehmer,J;Morrow,CS
据信，人类恶性肿瘤在很大程度上是由对 DNA 的直接化学或物理损伤，或促诱剂诱导的 DNA 序列复制/修复介导的修饰引起的，导致有害的遗传变化，开始逐步进展到异常生长控制 [1]。肿瘤进展的后续步骤可能是由维持基因组保真度的复制和修复系统完整性的变化（遗传介导）[2, 3] 或表观遗传调控影响（例如信号通路的改变）驱动的 [1, 4]。然而，起始的基因变化是不可逆的，并且可能会增加后续进展事件的可能性。因此，预防
Human malignancies are believed to be initiated in a large part by either direct chemical or physical damage to DNA, or replication/repair-mediated modification of the DNA sequence induced by promutagenic agents, resulting in deleterious genetic changes that begin a stepwise progression to abnormal growth control [1]. Later steps in the progression to neoplasia may be driven by changes in the integrity of replication and repair systems that maintain genomic fidelity (genetic mediation)[2, 3] or epigenetic regulatory influences such as alterations in signaling pathways [1, 4]. However, the initiating genetic changes are irreversible and may increase the probability of subsequent progression events. Hence, prevention