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Tau作为微管相关蛋白的作用：结构与功能方面

Role of Tau as a Microtubule-Associated Protein: Structural and Functional Aspects.

作者信息

Barbier Pascale, Zejneli Orgeta, Martinho Marlène, Lasorsa Alessia, Belle Valérie, Smet-Nocca Caroline, Tsvetkov Philipp O, Devred François, Landrieu Isabelle

机构信息

Fac Pharm, Aix Marseille Univ., Centre National de la Recherche Scientifique (CNRS), Inst Neurophysiopathol (INP), Fac Pharm, Marseille, France.

Univ. Lille, Centre National de la Recherche Scientifique (CNRS), UMR 8576, Unité de Glycobiologie Structurale et Fonctionnelle (UGSF), Lille, France.

出版信息

Front Aging Neurosci. 2019 Aug 7;11:204. doi: 10.3389/fnagi.2019.00204. eCollection 2019.

DOI:10.3389/fnagi.2019.00204
PMID:31447664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6692637/
Abstract

Microtubules (MTs) play a fundamental role in many vital processes such as cell division and neuronal activity. They are key structural and functional elements in axons, supporting neurite differentiation and growth, as well as transporting motor proteins along the axons, which use MTs as support tracks. Tau is a stabilizing MT associated protein, whose functions are mainly regulated by phosphorylation. A disruption of the MT network, which might be caused by Tau loss of function, is observed in a group of related diseases called tauopathies, which includes Alzheimer's disease (AD). Tau is found hyperphosphorylated in AD, which might account for its loss of MT stabilizing capacity. Since destabilization of MTs after dissociation of Tau could contribute to toxicity in neurodegenerative diseases, a molecular understanding of this interaction and its regulation is essential.

摘要

微管（MTs）在许多重要过程中发挥着基本作用，如细胞分裂和神经元活动。它们是轴突中的关键结构和功能元件，支持神经突的分化和生长，并沿着轴突运输运动蛋白，轴突利用微管作为支撑轨道。Tau是一种与微管稳定相关的蛋白质，其功能主要受磷酸化调节。在一组称为tau蛋白病的相关疾病中观察到微管网络的破坏，这可能是由Tau功能丧失引起的，其中包括阿尔茨海默病（AD）。在AD中发现Tau高度磷酸化，这可能解释了其微管稳定能力的丧失。由于Tau解离后微管的不稳定可能导致神经退行性疾病中的毒性，因此对这种相互作用及其调节的分子理解至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/2d9a4d4764e5/fnagi-11-00204-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/3a87bd246b45/fnagi-11-00204-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/429f0916daa6/fnagi-11-00204-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/a3590a8fa0b3/fnagi-11-00204-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/e9973ef0290b/fnagi-11-00204-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/2d9a4d4764e5/fnagi-11-00204-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/3a87bd246b45/fnagi-11-00204-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/429f0916daa6/fnagi-11-00204-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/a3590a8fa0b3/fnagi-11-00204-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/e9973ef0290b/fnagi-11-00204-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9634/6692637/2d9a4d4764e5/fnagi-11-00204-g0005.jpg

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