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Base excision repair and the central nervous system
- Source :
- Neuroscience. 145:1187-1200
- Publication Year :
- 2007
- Publisher :
- Elsevier BV, 2007.
-
Abstract
- Reactive oxygen species generated during normal cellular metabolism react with lipids, proteins, and nucleic acid. Evidence indicates that the accumulation of oxidative damage results in cellular dysfunction or deterioration. In particular, oxidative DNA damage can induce mutagenic replicative outcomes, leading to altered cellular function and/or cellular transformation. Additionally, oxidative DNA modifications can block essential biological processes, namely replication and transcription, triggering cell death responses. The major pathway responsible for removing oxidative DNA damage and restoring the integrity of the genome is base excision repair (BER). We highlight herein what is known about BER protein function(s) in the CNS, which in cooperation with the peripheral nervous system operates to control physical responses, motor coordination, and brain operation. Moreover, we describe evidence indicating that defective BER processing can promote post-mitotic (i.e. non-dividing) neuronal cell death and neurodegenerative disease. The focus of the review is on the core mammalian BER participants, i.e. the DNA glycosylases, AP endonuclease 1, DNA polymerase β, X-ray cross-complementing 1, and the DNA ligases.
- Subjects :
- Central Nervous System
Neurons
DNA Repair
biology
Cell Survival
DNA polymerase
DNA repair
General Neuroscience
NEIL1
Neurodegenerative Diseases
Base excision repair
Mitochondria
AP endonuclease
Oxidative Stress
XRCC1
chemistry.chemical_compound
DNA Repair Enzymes
chemistry
Biochemistry
DNA glycosylase
biology.protein
Animals
Humans
DNA
DNA Damage
Subjects
Details
- ISSN :
- 03064522
- Volume :
- 145
- Database :
- OpenAIRE
- Journal :
- Neuroscience
- Accession number :
- edsair.doi.dedup.....27bf9e24d873c994f6dd6afeadb16e92