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体外神经元分化过程中烷基化损伤修复的变化。

Changes in alkylation damage removal during in vitro neuronal differentiation.

作者信息

Czibula A, Leiker G, Raskó I

机构信息

Institute of Genetics, Hungarian Academy of Sciences, Szeged, Hungary.

出版信息

Acta Biol Hung. 1997;48(1):113-20.

PMID:9199706
Abstract

Mouse teratocarcinoma cell lines allow the analysis of very early commitment and differentiation events, that are likely to be similar to those operating in the early mouse embryo. We have previously characterised the excision repair capabilities of these cells after ultraviolet light irradiation and found that differentiation is accompanied by reduction of excision repair. In the present study we examine the operation of an other DNA repair pathway participating in the removal of alkylation damage. O6-alkylguanine-DNA alkyltransferase (ATase) activity was determined in undifferentiated and differentiated mouse P19 teratocarcinoma cell line. To obtain more information about regulation of ATase we transfected P19 cells with constructs harbouring a human ATase cDNA driven by a housekeeping promoter.

摘要

小鼠畸胎瘤细胞系有助于分析非常早期的定向分化事件,这些事件可能与早期小鼠胚胎中发生的事件相似。我们之前已经对这些细胞在紫外线照射后的切除修复能力进行了表征,发现分化伴随着切除修复能力的降低。在本研究中,我们研究了另一种参与去除烷基化损伤的DNA修复途径的运作情况。在未分化和分化的小鼠P19畸胎瘤细胞系中测定了O6-烷基鸟嘌呤-DNA烷基转移酶(ATase)的活性。为了获得更多关于ATase调控的信息,我们用含有由管家启动子驱动的人ATase cDNA的构建体转染了P19细胞。

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