蛋白质L-异天冬氨酰甲基转移酶在神经退行性疾病病理生理学中的作用:与突触功能相关的可能底物。

IF 4.4 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Neurochemistry international Pub Date : 2023-11-01 DOI:10.1016/j.neuint.2023.105606
Sirui Zhou , Yancheng Zhou , Wanyu Zhong , Zhonghao Su , Zhenxia Qin
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引用次数: 0

摘要

突触功能障碍是阿尔茨海默病(AD)、帕金森病(PD)、辛廷顿病(HD)和肌萎缩侧索硬化症(ALS)等神经退行性疾病(ND)的典型病理生理变化,涉及蛋白质翻译后修饰(PTM),包括通过天冬氨酸异构化或天冬酰胺脱酰胺形成的L-异天冬氨酸(L-isoAsp)。蛋白质L-异天冬氨酰甲基转移酶(PIMT)可以修复L-异天冬酶的形成。一些突触蛋白已被鉴定为PIMT潜在底物,在确保突触功能方面发挥着重要作用。在这篇综述中,我们讨论了某些突触蛋白作为PIMT底物在神经退行性疾病中的作用,从而为NDs的治疗提供了以突触为中心的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Involvement of protein L-isoaspartyl methyltransferase in the physiopathology of neurodegenerative diseases: Possible substrates associated with synaptic function

Synaptic dysfunction is a typical pathophysiologic change in neurodegenerative diseases (NDs) such as Alzheimer's disease (AD), Parkinson's disease (PD), Hintington's disease (HD) and amyotrophic lateral sclerosis (ALS), which involves protein post-translational modifications (PTMs) including L-isoaspartate (L-isoAsp) formed by isomerization of aspartate or deamidation of asparagine. The formation of L-isoAsp could be repaired by protein L-isoaspartyl methyltransferase (PIMT). Some synaptic proteins have been identified as PIMT potential substrates and play an essential role in ensuring synaptic function. In this review, we discuss the role of certain synaptic proteins as PIMT substrates in neurodegenerative disease, thus providing therapeutic synapse-centered targets for the treatment of NDs.

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来源期刊
Neurochemistry international
Neurochemistry international 医学-神经科学
CiteScore
8.40
自引率
2.40%
发文量
128
审稿时长
37 days
期刊介绍: Neurochemistry International is devoted to the rapid publication of outstanding original articles and timely reviews in neurochemistry. Manuscripts on a broad range of topics will be considered, including molecular and cellular neurochemistry, neuropharmacology and genetic aspects of CNS function, neuroimmunology, metabolism as well as the neurochemistry of neurological and psychiatric disorders of the CNS.
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