Base excision repair in physiology and pathology of the central nervous system.

Base excision repair in physiology and pathology of the central nervous system.
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DOI:
10.3390/ijms131216172
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发表时间:
2012-11-30
影响因子:
5.6
通讯作者:
van Loon B
van Loon B
中科院分区:
生物学2区
文献类型:
--
作者:
Bosshard M;Markkanen E;van Loon B

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相对低水平的抗氧化酶和高氧代谢导致中枢神经系统组织中形成大量氧化DNA病变。由于持续的基因毒性应激,DNA损伤的积累与衰老和各种神经退行性疾病的发展有关。不同的DNA修复途径已经进化到成功地作用于受损的DNA和防止基因组不稳定。主要和必要的DNA修复途径去除小的DNA碱基病变是碱基切除修复(BER)。在这篇综述中,我们将讨论目前关于BER蛋白参与维持大脑不同区域遗传稳定性的知识,以及这些蛋白水平的变化如何促进衰老和神经退行性疾病的发生。
Relatively low levels of antioxidant enzymes and high oxygen metabolism result in formation of numerous oxidized DNA lesions in the tissues of the central nervous system. Accumulation of damage in the DNA, due to continuous genotoxic stress, has been linked to both aging and the development of various neurodegenerative disorders. Different DNA repair pathways have evolved to successfully act on damaged DNA and prevent genomic instability. The predominant and essential DNA repair pathway for the removal of small DNA base lesions is base excision repair (BER). In this review we will discuss the current knowledge on the involvement of BER proteins in the maintenance of genetic stability in different brain regions and how changes in the levels of these proteins contribute to aging and the onset of neurodegenerative disorders.
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