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APE/Ref-1在中枢神经系统氧化应激反应中的保护作用 被引量:3

Protect Effects of APE/Ref-1 on Free Radicals Induced Central Nervous System Diseases
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摘要 化学性质活泼的自由基(freeradicals)在保持产生和清除平衡的稳衡性动态下能履行正常的生理功能,但超过生物体的清除能力则可导致多种疾病.无嘌呤无嘧啶核酸内切酶氧化还原因子1(apurinicapyrimidinicendonucleaseredoxfactor1,APERef1)是一种体内分布广泛的多功能蛋白质,通过修复DNA的无嘌呤无嘧啶(apurinicapyrimidinic,AP)部位参与DNA的碱基切除修复(baseexcisionrepair,BER).APERef1还可通过还原许多转录因子的半胱氨酸残基使之易于与DNA结合而调控真核细胞的基因表达.APERef1的抗细胞凋亡作用使其在自由基所致中枢神经系统病变如脑缺血再灌注损伤、神经退行性病变、脑动脉粥样硬化中发挥了重要作用. Free radicals which have reactive chemical properties can perform diverse physiological functions when the balance of production and scavenging of them have been maintained. But when the amount of free radical is exceedes the clearance capacity of body, free radicals may induce a variety of diseases. Apurinic/apyrimidinic endonuclease/redox-factor 1 (APE/Ref-1) is a multifunctional protein in the DNA base excision repair (BER) pathway that is responsible for repairing apurinic/apyrimidinic (AP) sites in DNA. APE/Ref-1 can also regulates eukaryotic gene expression because it has been shown to activate numerous transcription factors and facilitate their DNA binding via the reduction of a cysteine residue. APE/Ref-1 plays a crucial role in the free radical induced central nervous system diseases such as focal cerebral ischemia-reperfusion injury, neurodegenerative diseases and cerebral atherosclerosis depending on its function of anti-apoptosis.
作者 陈欣 刘艳霞
出处 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2006年第5期355-359,共5页 Chinese Journal of Biochemistry and Molecular Biology
关键词 自由基 无嘌呤/无嘧啶核酸内切酶/氧化还原因子1 中枢神经系统病变 free radicals endonuclease/redox-factor 1 CNS diseases
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