A short review on the implications of base excision repair pathway for neurons: Relevance to neurodegenerative diseases
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Date
2014
Journal Title
Journal ISSN
Volume Title
Publisher
Elsevier
Abstract
Oxidative DNA damage results from the attack by reactive oxygen and nitrogen species (ROS/RNS) on human genome. This includes base modifications such as oxidized bases, abasic (AP) sites, and single-strand breaks (SSBs), all of which are repaired by the base excision repair (BER) pathway, one among the six known repair pathways. BER-pathway in mammalian cells involves several evolutionarily conserved proteins and is also linked to genome replication and transcription. The BER-pathway enzymes, namely, DNA glycosylases (DGs) and the end-processing proteins such as abasic endonuclease (APE1), form complexes with downstream repair enzymes via protein-protein and DNA-protein interactions. An emerging concept for BER proteins is their involvement in non-canonical functions associated to RNA metabolism, which is opening new interesting perspectives. Various mechanisms that are underlined in maintaining neuronal cell genome integrity are identified, but are inconclusive in providing protection against oxidative damage in neurodegenerative disorders, main emphasis is given towards the role played by the proteins of BER-pathway that is discussed. In addition, mechanisms of action of BER-pathway in nuclear vs. mitochondria as well as the non-canonical functions are discussed in connection to human neurodegenerative diseases. ? 2013 ? Elsevier B.V. and Mitochondria Research Society. All rights reserved.
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Keywords
DNA (apurinic or apyrimidinic site) lyase, DNA glycosyltransferase, DNA polymerase, Endonuclease, Flap endonuclease, Mitochondrial protein, Nuclear protein, Phosphodiesterase I, Protein DNA2, Protein EXOG, RNA, Unclassified drug, XRCC1 protein, DNA, Protein binding, Reactive nitrogen species, Reactive oxygen metabolite;
Citation
Mantha, A. K., Sarkar, B., & Tell, G. (2014). A short review on the implications of base excision repair pathway for neurons: Relevance to neurodegenerative diseases. Mitochondrion, 16, 38-49. doi: 10.1016/j.mito.2013.10.007