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钙离子稳态与内质网应激:钙信号的综合观点

Ca(2+) homeostasis and endoplasmic reticulum (ER) stress: An integrated view of calcium signaling.

作者信息

Krebs Joachim, Agellon Luis B, Michalak Marek

机构信息

NMR-based Structural Biology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.

School of Dietetics and Human Nutrition, McGill University, Ste. Anne de Bellevue, Quebec H9X 3V9, Canada.

出版信息

Biochem Biophys Res Commun. 2015 Apr 24;460(1):114-21. doi: 10.1016/j.bbrc.2015.02.004.

Abstract

Cellular Ca(2+) homeostasis is maintained through the integrated and coordinated function of Ca(2+) transport molecules, Ca(2+) buffers and sensors. These molecules are associated with the plasma membrane and different cellular compartments, such as the cytoplasm, nucleus, mitochondria, and cellular reticular network, including the endoplasmic reticulum (ER) to control free and bound Ca(2+) levels in all parts of the cell. Loss of nutrients/energy leads to the loss of cellular homeostasis and disruption of Ca(2+) signaling in both the reticular network and cytoplasmic compartments. As an integral part of cellular physiology and pathology, this leads to activation of ER stress coping responses, such as the unfolded protein response (UPR), and mobilization of pathways to regain ER homeostasis.

摘要

细胞内钙离子稳态通过钙离子转运分子、钙离子缓冲剂和传感器的整合与协调功能得以维持。这些分子与质膜以及不同的细胞区室相关联,如细胞质、细胞核、线粒体和细胞网状网络,包括内质网(ER),以控制细胞各部分游离和结合的钙离子水平。营养物质/能量的丧失会导致细胞内稳态的丧失以及网状网络和细胞质区室中钙离子信号的破坏。作为细胞生理和病理的一个组成部分,这会导致内质网应激应对反应的激活,如未折叠蛋白反应(UPR),以及动员恢复内质网稳态的途径。

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