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应激对高尔基体结构的改变:与神经退行性变有关联?

Alteration of Golgi Structure by Stress: A Link to Neurodegeneration?

作者信息

Alvarez-Miranda Eduardo A, Sinnl Markus, Farhan Hesso

机构信息

Department of Industrial Engineering, Universidad de Talca Curicó, Chile.

Department of Statistics and Operations Research, University of Vienna Vienna, Austria.

出版信息

Front Neurosci. 2015 Nov 12;9:435. doi: 10.3389/fnins.2015.00435. eCollection 2015.

DOI:10.3389/fnins.2015.00435
PMID:26617486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4641911/
Abstract

The Golgi apparatus is well-known for its role as a sorting station in the secretory pathway as well as for its role in regulating post-translational protein modification. Another role for the Golgi is the regulation of cellular signaling by spatially regulating kinases, phosphatases, and GTPases. All these roles make it clear that the Golgi is a central regulator of cellular homeostasis. The response to stress and the initiation of adaptive responses to cope with it are fundamental abilities of all living cells. It was shown previously that the Golgi undergoes structural rearrangements under various stress conditions such as oxidative or osmotic stress. Neurodegenerative diseases are also frequently associated with alterations of Golgi morphology and many stress factors have been described to play an etiopathological role in neurodegeneration. It is however unclear whether the stress-Golgi connection plays a role in neurodegenerative diseases. Using a combination of bioinformatics modeling and literature mining, we will investigate evidence for such a tripartite link and we ask whether stress-induced Golgi arrangements are cause or consequence in neurodegeneration.

摘要

高尔基体作为分泌途径中的分拣站以及调节翻译后蛋白质修饰的作用而广为人知。高尔基体的另一个作用是通过在空间上调节激酶、磷酸酶和GTP酶来调节细胞信号传导。所有这些作用都清楚地表明,高尔基体是细胞稳态的核心调节因子。对压力的反应以及启动适应性反应以应对压力是所有活细胞的基本能力。先前的研究表明,在各种应激条件下,如氧化应激或渗透应激,高尔基体都会发生结构重排。神经退行性疾病也经常与高尔基体形态的改变有关,并且已经描述了许多应激因素在神经退行性变中发挥病因学作用。然而,尚不清楚应激与高尔基体之间的联系是否在神经退行性疾病中起作用。通过结合生物信息学建模和文献挖掘,我们将研究这种三方联系的证据,并探讨应激诱导的高尔基体排列在神经退行性变中是原因还是结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/3236737668b7/fnins-09-00435-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/ecd48310058d/fnins-09-00435-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/4c6857cb481d/fnins-09-00435-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/fe3ec17b6683/fnins-09-00435-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/3236737668b7/fnins-09-00435-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/ecd48310058d/fnins-09-00435-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/4c6857cb481d/fnins-09-00435-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/fe3ec17b6683/fnins-09-00435-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c66/4641911/3236737668b7/fnins-09-00435-g0004.jpg

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