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细菌硝基还原酶在转基因小鼠中的表达导致前体药物CB1954对特定细胞的杀伤作用。

The expression of bacterial nitroreductase in transgenic mice results in specific cell killing by the prodrug CB1954.

作者信息

Drabek D, Guy J, Craig R, Grosveld F

机构信息

Department of Cell Biology and Genetics, Institute of Cell Biology, Rotterdam, The Netherlands.

出版信息

Gene Ther. 1997 Feb;4(2):93-100. doi: 10.1038/sj.gt.3300366.

Abstract

The enzyme nitroreductase, isolated from Escherichia coli B, converts CB1954 ((5-aziridin-1-yl)-2,4-dinitro-benzamide) into a cytotoxic DNA interstrand cross-linking agent. The E. coli B gene (nfnB, NTR) encoding nitroreductase (NTR) was cloned into eukaryotic expression vectors. When driven by a CMV promoter, 5-10% of the stably transfected mouse fibroblasts expressed the NTR enzyme. These cells were killed at a concentration of 20 microM CB1954 in comparison to nonexpressing cells which were killed at a much higher concentration (500 microM). We subsequently generated transgenic mice to test the prodrug system in vivo. Nitroreductase was expressed specifically in T cells driven by the control elements of the human CD2 locus. Upon CB1954 treatment, transgenic mice show extensive cell depletion in thymus and spleen (14-16% of normal cell numbers), whereas all other tissues are unaffected by prodrug administration. These results raise the possibility of using the NTR gene in anticancer therapy.

摘要

从大肠杆菌B中分离出的硝基还原酶可将CB1954((5-氮丙啶-1-基)-2,4-二硝基苯甲酰胺)转化为一种具有细胞毒性的DNA链间交联剂。编码硝基还原酶(NTR)的大肠杆菌B基因(nfnB,NTR)被克隆到真核表达载体中。当由巨细胞病毒(CMV)启动子驱动时,5-10%的稳定转染小鼠成纤维细胞表达NTR酶。与在高得多的浓度(500微摩尔)下才被杀死的非表达细胞相比,这些细胞在20微摩尔CB1954的浓度下就被杀死。我们随后培育出转基因小鼠以在体内测试前药系统。在人CD2基因座的调控元件驱动下,硝基还原酶在T细胞中特异性表达。经CB1954处理后,转基因小鼠的胸腺和脾脏出现广泛的细胞耗竭(正常细胞数量的14-16%),而所有其他组织不受前药给药的影响。这些结果增加了在抗癌治疗中使用NTR基因的可能性。

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