Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.70733
R. Carter, J. Parsons
Genome integrity is under constant threat from cellular reactive oxygen species generated by endogenous and exogenous mutagens. The base excision repair (BER) pathway consequently plays a crucial role in the repair of DNA base damage, sites of base loss and DNA single strand breaks that can cause genome instability and ultimately the development of human diseases, including premature ageing, neurodegenerative disorders and cancer. Proteins within the base excision repair pathway are increasingly being found to be regulated and controlled by post-translational modifications, and indeed ubiquitination per - forms a key role in the maintenance of repair protein levels but may also impact on protein activity and cellular localisation. This process is therefore important in maintaining an effi - cient cellular DNA damage response, and if not accurately controlled, can cause DNA damage accumulation and promote mutagenesis and genomic instability. In this chapter, we will present up-to-date information on the evidence of ubiquitination of base excision repair proteins, the enzymes involved and the molecular and cellular consequences of this process. towards these specific proteins stages
基因组的完整性不断受到内源和外源突变物产生的细胞活性氧的威胁。因此，碱基切除修复（BER）途径在修复 DNA 碱基损伤、碱基缺失位点和 DNA 单链断裂方面发挥着至关重要的作用，这些损伤和断裂可导致基因组不稳定，最终引发人类疾病，包括早衰、神经退行性疾病和癌症。人们发现，碱基切除修复途径中的蛋白质越来越多地受到翻译后修饰的调节和控制，事实上，泛素化不仅在维持修复蛋白质水平方面发挥着关键作用，还可能对蛋白质的活性和细胞定位产生影响。因此，这一过程对于维持高效的细胞 DNA 损伤反应非常重要，如果不能准确控制，就会造成 DNA 损伤积累，促进突变和基因组不稳定性。在本章中，我们将介绍有关碱基切除修复蛋白泛素化的证据、所涉及的酶以及这一过程的分子和细胞后果的最新信息。
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