棕榈酰化
神经退行性变
生物
细胞生物学
淀粉样前体蛋白
亨廷顿蛋白
神经科学
阿尔茨海默病
突变体
生物化学
疾病
酶
半胱氨酸
医学
基因
病理
作者
Jakub Włodarczyk,Raja Bhattacharyya,Kim Doré,Gary P. H. Ho,Dale D. O. Martin,Rebeca Mejı́as,Karin Hochrainer
标识
DOI:10.1523/jneurosci.1225-24.2024
摘要
Palmitoylation, a lipid-based posttranslational protein modification, plays a crucial role in regulating various aspects of neuronal function through altering protein membrane-targeting, stabilities, and protein–protein interaction profiles. Disruption of palmitoylation has recently garnered attention as disease mechanism in neurodegeneration. Many proteins implicated in neurodegenerative diseases and associated neuronal dysfunction, including but not limited to amyloid precursor protein, β-secretase (BACE1), postsynaptic density protein 95, Fyn, synaptotagmin-11, mutant huntingtin, and mutant superoxide dismutase 1, undergo palmitoylation, and recent evidence suggests that altered palmitoylation contributes to the pathological characteristics of these proteins and associated disruption of cellular processes. In addition, dysfunction of enzymes that catalyze palmitoylation and depalmitoylation has been connected to the development of neurological disorders. This review highlights some of the latest advances in our understanding of palmitoylation regulation in neurodegenerative diseases and explores potential therapeutic implications.
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