Revisiting the rodent repairadox
Revisiting the rodent repairadox
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DOI：
10.1002/em.1057
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发表时间：
2001-01-01
影响因子：
2.8
通讯作者：
Hanawalt, PC
中科院分区：
文献类型：
--
作者：
Hanawalt, PC
培养的啮齿动物和人类细胞在暴露于紫外线（UV）后通常显示出相似的克隆存活特征。然而，与人类细胞相比，来自小鼠、大鼠和仓鼠的培养细胞通常缺乏对由UV产生的最突出的DNA损伤（环丁烷嘧啶二聚体）的切除修复。根据最近对核苷酸切除修复控制的研究，我们开始了解这种所谓的“修复剂”的基础。“这个问题的解决很重要，因为啮齿动物在遗传毒理学中被广泛用作人类的替代品。本文将回顾我们对啮齿动物DNA修复的理解的演变，并将“重温”我与我的研究生导师和受人尊敬的同事迪克·塞特洛的早期交往，以纪念他80岁生日时的荣誉。Environ.摩尔变异体(C)2001 Wiley-Liss，Inc.
Cultured rodent and human cells typically display similar clonal survival characteristics following exposure to ultraviolet light (UV). However, compared to human cells, cultured cells from mice, rats, and hamsters are generally deficient in excision repair of the most prominent DNA lesion produced by UV, the cyclobutane pyrimidine dimer. In light of recent studies on the control of nucleotide excision repair, we are beginning to understand the basis for this so-called "repairadox." The resolution of this issue is important because rodents are so widely employed as surrogates for humans in genetic toxicology. This article will review the evolution in our understanding of rodent DNA repair and will also "revisit" my early association with my graduate mentor and esteemed colleague, Dick Setlow, in his honor upon the attainment of his 80th birthday. Environ. Mol. Mutagen. (C) 2001 Wiley-Liss, Inc.