神经退行性变
棕榈酰化
肌萎缩侧索硬化
相扑蛋白
生物
蛋白质聚集
泛素
神经科学
疾病
细胞生物学
医学
生物化学
病理
半胱氨酸
基因
酶
作者
Sadat Shafi,Archu Singh,Paras Gupta,Pooja A. Chawla,Faizana Fayaz,Anil Kumar Sharma,Faheem Hyder Pottoo
出处
期刊:Cns & Neurological Disorders-drug Targets
[Bentham Science]
日期:2021-05-17
卷期号:20 (1): 54-67
被引量:8
标识
DOI:10.2174/1871527319666200903162200
摘要
Neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Amyotrophic Lateral Sclerosis (ALS) and Huntington's Disease (HD), are characterized by progressive neuronal dysfunction and death. Recent studies have established detrimental modifications in the structure and function of brain proteins, which stimulate their aggregation, misfolding and deposition in and around the neurons an important hallmark of neurodegenerative diseases. Post-Translational Modification (PTM) of proteins, including phosphorylation, acetylation, glycosylation, palmitoylation, SUMOylation, and ubiquitination, are important regulators of protein characteristics, including stability, intracellular distribution, activity, interactions, aggregation and clearance. Despite clear evidence that altered protein modifications emerging from impromptu chemical modifications to side chains of amino acid are associated with neurodegeneration, the underlying mechanisms that promote aberrant PTM remain poorly understood. Therefore, elucidating PTM of specific disease-associated proteins can prove to be a significant step in evaluating the functional alteration of proteins and their association with neurodegeneration. This review describes how aberrant PTM of various proteins is linked with the neurodegenerative disease pathogenesis, as well as molecular strategies targeting these modifications for treating such diseases, which are yet incurable.
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