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与神经退行性疾病相关的蛋白质:与DNA修复的联系

Proteins Associated with Neurodegenerative Diseases: Link to DNA Repair.

作者信息

Khodyreva Svetlana N, Dyrkheeva Nadezhda S, Lavrik Olga I

机构信息

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Sciences, 8 Akad. Lavrentyeva pr., Novosibirsk 630090, Russia.

Faculty of Natural Sciences, Novosibirsk State University, 2 Pirogova Str., Novosibirsk 630090, Russia.

出版信息

Biomedicines. 2024 Dec 11;12(12):2808. doi: 10.3390/biomedicines12122808.

DOI:10.3390/biomedicines12122808
PMID:39767715
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11673744/
Abstract

The nervous system is susceptible to DNA damage and DNA repair defects, and if DNA damage is not repaired, neuronal cells can die, causing neurodegenerative diseases in humans. The overall picture of what is known about DNA repair mechanisms in the nervous system is still unclear. The current challenge is to use the accumulated knowledge of basic science on DNA repair to improve the treatment of neurodegenerative disorders. In this review, we summarize the current understanding of the function of DNA damage repair, in particular, the base excision repair and double-strand break repair pathways as being the most important in nervous system cells. We summarize recent data on the proteins involved in DNA repair associated with neurodegenerative diseases, with particular emphasis on PARP1 and ND-associated proteins, which are involved in DNA repair and have the ability to undergo liquid-liquid phase separation.

摘要

神经系统易受DNA损伤和DNA修复缺陷的影响,如果DNA损伤得不到修复,神经元细胞可能会死亡,从而导致人类神经退行性疾病。目前对于神经系统中DNA修复机制的整体认识仍不明确。当前的挑战是利用积累的关于DNA修复的基础科学知识来改善神经退行性疾病的治疗。在这篇综述中,我们总结了目前对DNA损伤修复功能的理解,特别是碱基切除修复和双链断裂修复途径在神经细胞中最为重要。我们总结了与神经退行性疾病相关的参与DNA修复的蛋白质的最新数据,特别强调了PARP1和与神经退行性疾病相关的蛋白质,它们参与DNA修复并具有发生液-液相分离的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5876/11673744/24d13d455348/biomedicines-12-02808-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5876/11673744/46510e0cce15/biomedicines-12-02808-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5876/11673744/51a618f28fad/biomedicines-12-02808-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5876/11673744/24d13d455348/biomedicines-12-02808-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5876/11673744/46510e0cce15/biomedicines-12-02808-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5876/11673744/51a618f28fad/biomedicines-12-02808-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5876/11673744/24d13d455348/biomedicines-12-02808-g003.jpg

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本文引用的文献

1
TDP-43 nuclear condensation and neurodegenerative proteinopathies.TDP-43 核凝聚与神经退行性蛋白病。
Trends Neurosci. 2024 Nov;47(11):849-850. doi: 10.1016/j.tins.2024.09.003. Epub 2024 Sep 25.
2
Alpha-synuclein modulates the repair of genomic DNA double-strand breaks in a DNA-PK-regulated manner.α-突触核蛋白以依赖于 DNA-PK 的方式调节基因组 DNA 双链断裂的修复。
Neurobiol Dis. 2024 Oct 15;201:106675. doi: 10.1016/j.nbd.2024.106675. Epub 2024 Sep 19.
3
Divalent and multivalent cations control liquid-like assembly of poly(ADP-ribosyl)ated PARP1 into multimolecular associates in vitro.
二价和多价阳离子控制聚(ADP-核糖基)化 PARP1 在体外形成多分子聚集体的液态样组装。
Commun Biol. 2024 Sep 15;7(1):1148. doi: 10.1038/s42003-024-06811-4.
4
Activation of multifunctional DNA repair APE1/Ref-1 enzyme by the dietary phytochemical Ferulic acid protects human neuroblastoma SH-SY5Y cells against Aβ(25-35)-induced oxidative stress and inflammatory responses.膳食植物化学物阿魏酸通过激活多功能 DNA 修复 APE1/Ref-1 酶来保护人神经母细胞瘤 SH-SY5Y 细胞免受 Aβ(25-35)诱导的氧化应激和炎症反应。
Mitochondrion. 2024 Nov;79:101947. doi: 10.1016/j.mito.2024.101947. Epub 2024 Aug 14.
5
Tau beyond Tangles: DNA Damage Response and Cytoskeletal Protein Crosstalk on Neurodegeneration.tau 超越缠结:DNA 损伤反应和细胞骨架蛋白在神经退行性变中的相互作用。
Int J Mol Sci. 2024 Jul 19;25(14):7906. doi: 10.3390/ijms25147906.
6
Regulation of DNA damage response by RNA/DNA-binding proteins: Implications for neurological disorders and aging.RNA/DNA结合蛋白对DNA损伤反应的调控:对神经疾病和衰老的影响
Ageing Res Rev. 2024 Sep;100:102413. doi: 10.1016/j.arr.2024.102413. Epub 2024 Jul 19.
7
DNA Damage and Chromatin Rearrangement Work Together to Promote Neurodegeneration.DNA损伤与染色质重排共同作用促进神经退行性变。
Mol Neurobiol. 2025 Jan;62(1):1282-1290. doi: 10.1007/s12035-024-04331-0. Epub 2024 Jul 8.
8
CS proteins and ubiquitination: orchestrating DNA repair with transcription and cell division.CS 蛋白与泛素化:通过转录和细胞分裂调控 DNA 修复。
Trends Cell Biol. 2024 Oct;34(10):882-895. doi: 10.1016/j.tcb.2024.06.002. Epub 2024 Jun 22.
9
Liquid-liquid phase separation induced by crowding condition affects amyloid-β aggregation mechanism.拥挤环境诱导的液-液相分离影响淀粉样β聚集机制。
Soft Matter. 2024 Jul 10;20(27):5331-5342. doi: 10.1039/d4sm00470a.
10
TDP43 interacts with MLH1 and MSH6 proteins in a DNA damage-inducible manner.TDP43 以一种 DNA 损伤诱导的方式与 MLH1 和 MSH6 蛋白相互作用。
Mol Brain. 2024 Jun 5;17(1):32. doi: 10.1186/s13041-024-01108-3.