钙网蛋白通过内质网应激介导细胞凋亡的分子机制

生物技术通报 ›› 2013, Vol. 0 ›› Issue (10): 24-27.

钙网蛋白通过内质网应激介导细胞凋亡的分子机制

吴薇,刘朝奇

（三峡大学分子生物学研究所，宜昌 443002）

收稿日期:2013-04-18 修回日期:2013-10-15 出版日期:2013-10-14 发布日期:2013-10-15
作者简介:刘朝奇，男，博士，教授，硕士生导师，研究方向：肿瘤分子免疫学；E-mail: zqliu@ctgu.edu.cn
基金资助:
吴薇，女，硕士研究生，研究方向：肿瘤分子免疫学；E-mail ：lezhiweiwei@163.com

Calreticulin and Apoptosis Mediated by Endoplasmic Reticulum Stress

Wu Wei, Liu Chaoqi

（Institute of Molecular Biology，Three Gorges University，Yichang 443002）

Received:2013-04-18 Revised:2013-10-15 Published:2013-10-14 Online:2013-10-15

摘要/Abstract

摘要： 钙网蛋白（Calreticulin，CRT）是46 kD 大小的内质网管腔蛋白，具有分子伴侣活性、调节内钙稳态以及细胞凋亡等多种生物学功能。内质网应激（Endoplasmic reticulum stress，ERS）是内质网生理功能发生紊乱的一种亚细胞器病理过程，早期反应是可逆的，但随着细胞损伤加重将会导致细胞的凋亡，即为内质网应激启动的细胞凋亡。新的研究显示，CRT 在该凋亡途径中扮演着重要角色。从三方面综述两者间的相互关系，以期为该方向的研究人员提供一些参考。

关键词: 钙网蛋白, 分子伴侣蛋白, 内质网应激, 细胞凋亡

Abstract: Calreticulin（CRT）is a 46 kD endoplasmic reticulum luminal protein and has various biological functions including chaperone activity, regulation of Ca2+ homeostasis, cell apoptosis. Endoplasmic reticulum stress（ERS）is pathological changes of subcellular organelles, early time of ERS can be reversed, as the time go, cellular damage is more and more serious result in apoptosis. New research shows that CRT plays an important role in apoptosis mediated by endoplasmic reticulum stress. This review explained clearly the interrelation between them and was expected to provide some information for the study.

Key words: Calreticulin, Chaperone, Endoplasmic reticulum stress, Cell apoptosis

吴薇,刘朝奇. 钙网蛋白通过内质网应激介导细胞凋亡的分子机制[J]. 生物技术通报, 2013, 0(10): 24-27.

Wu Wei Liu Chaoqi. Calreticulin and Apoptosis Mediated by Endoplasmic Reticulum Stress [J]. Biotechnology Bulletin, 2013, 0(10): 24-27.

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