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本文引用的文献

1
An Endosomal NAADP-Sensitive Two-Pore Ca Channel Regulates ER-Endosome Membrane Contact Sites to Control Growth Factor Signaling.一种内体性对NAADP敏感的双孔钙通道调节内质网-内体膜接触位点以控制生长因子信号传导。
Cell Rep. 2017 Feb 14;18(7):1636-1645. doi: 10.1016/j.celrep.2017.01.052.
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Tuning the ion selectivity of two-pore channels.调节双孔通道的离子选择性。
Proc Natl Acad Sci U S A. 2017 Jan 31;114(5):1009-1014. doi: 10.1073/pnas.1616191114. Epub 2017 Jan 17.
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High resolution structural evidence suggests the Sarcoplasmic Reticulum forms microdomains with Acidic Stores (lysosomes) in the heart.高分辨率结构证据表明,心肌中的肌浆网与酸性储存器(溶酶体)形成微区。
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Inhibition of Transient Receptor Potential Channel Mucolipin-1 (TRPML1) by Lysosomal Adenosine Involved in Severe Combined Immunodeficiency Diseases.溶酶体腺苷对瞬时受体电位通道黏脂素-1(TRPML1)的抑制作用与重症联合免疫缺陷病有关。
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Intracellular TRPA1 mediates Ca2+ release from lysosomes in dorsal root ganglion neurons.细胞内的瞬时受体电位锚蛋白1(TRPA1)介导背根神经节神经元溶酶体释放钙离子(Ca2+)。
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Determining the Roles of Inositol Trisphosphate Receptors in Neurodegeneration: Interdisciplinary Perspectives on a Complex Topic.确定三磷酸肌醇受体在神经退行性变中的作用:一个复杂主题的跨学科视角。
Mol Neurobiol. 2017 Nov;54(9):6870-6884. doi: 10.1007/s12035-016-0205-8. Epub 2016 Oct 22.
8
Calcium at the Center of Cell Signaling: Interplay between Endoplasmic Reticulum, Mitochondria, and Lysosomes.细胞信号传导核心的钙:内质网、线粒体和溶酶体之间的相互作用
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BK channel agonist represents a potential therapeutic approach for lysosomal storage diseases.BK通道激动剂是溶酶体贮积症的一种潜在治疗方法。
Sci Rep. 2016 Sep 27;6:33684. doi: 10.1038/srep33684.
10
Endo-lysosomal TRP mucolipin-1 channels trigger global ER Ca2+ release and Ca2+ influx.内质网-溶酶体瞬时受体电位黏脂蛋白-1通道触发内质网Ca2+的整体释放及Ca2+内流。
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神经退行性变中的溶酶体钙

Lysosomal Calcium in Neurodegeneration.

作者信息

Feng Xinghua, Yang Junsheng

机构信息

Collaborative Innovation Center of Yangtze River Delta Region Green Pharmaceuticals, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.

The Department of Molecular, Cellular, and Developmental Biology, University of Michigan, 3089 Natural Science Building (Kraus), 830 North University, Ann Arbor, MI 48109, USA.

出版信息

Messenger (Los Angel). 2016 Jun;5(1-2):56-66. doi: 10.1166/msr.2016.1055. Epub 2016 Jun 1.

DOI:10.1166/msr.2016.1055
PMID:29082116
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5659362/
Abstract

Lysosomes are the central organelles responsible for macromolecule recycling in the cell. Lysosomal dysfunction is the primary cause of lysosomal storage diseases (LSDs), and contributes significantly to the pathogenesis of common neurodegenerative diseases. The lysosomes are also intracellular stores for calcium ions, one of the most common second messenger in the cell. Lysosomal Ca is required for diverse cellular processes including signal transduction, vesicular trafficking, autophagy, nutrient sensing, exocytosis, and membrane repair. In this review, we first summarize some recent progresses in the studies of lysosome Ca regulation, with a focus on the newly discovered lysosomal Ca channels and the mechanisms of lysosomal Ca store refilling. We then discuss how defects in lysosomal Ca release and store maintenance cause lysosomal dysfunction and neurodegeneration.

摘要

溶酶体是细胞内负责大分子循环利用的核心细胞器。溶酶体功能障碍是溶酶体贮积症(LSDs)的主要病因,并且在常见神经退行性疾病的发病机制中起重要作用。溶酶体也是细胞内钙离子的储存库,钙离子是细胞中最常见的第二信使之一。溶酶体钙参与多种细胞过程,包括信号转导、囊泡运输、自噬、营养感知、胞吐作用和膜修复。在本综述中,我们首先总结溶酶体钙调节研究的一些最新进展,重点关注新发现的溶酶体钙通道以及溶酶体钙库再填充机制。然后我们讨论溶酶体钙释放和储存维持缺陷如何导致溶酶体功能障碍和神经退行性变。