Significance of ER Ca2+ outflow during myogenesis
Significance of ER Ca2+ outflow during myogenesis
复制标题
肌生成过程中 ER Ca2 流出的意义
DOI：
10.1080/19336950.2015.1069504
复制
发表时间：
2015
期刊：
影响因子：
3.3
通讯作者：
N. Morishima and K. Nakanishi
中科院分区：
文献类型：
--
作者：
K. Nakanishi;K. Kakiguchi;S. Yonemura;A. Nakano;and N. Morishima;N. Morishima and K. Nakanishi
细胞内Ca ~（2+）动态调节细胞的各种功能。正如Ebashi的经典研究所报道的，1骨骼肌收缩受肌浆网释放的胞质Ca 2+调节，后者反过来激活肌钙蛋白C。由于细胞内Ca ~（2+）可以激活依赖Ca ~（2+）的蛋白质，从而调节细胞的活动和功能，因此Ca ~（2+）的作用在基础生物医学研究中引起了广泛的关注。近年来的研究表明，内质网（endoplasmic reticulum，ER）中Ca ~（2+）的释放和细胞外Ca ~（2+）的摄取是导致细胞内Ca ~（2+）增加的重要原因。当ER Ca 2+通过ER Ca 2+通道释放到胞质溶胶中时，在ER中同时发生Ca 2+耗竭。ER Ca 2+耗竭对细胞有潜在危害，因为它干扰了在粗糙ER上合成的蛋白质的正确折叠，这是由于ER Ca 2+依赖性分子伴侣（例如钙网蛋白和钙连接蛋白）的功能障碍。ER应激是一种细胞条件，其中错误折叠的蛋白质在ER中积累。2除了内质网Ca ~（2+）耗竭外，各种其他因素（如氧化应激、葡萄糖缺乏或蛋白质合成负担重）也可引起内质网应激。3我们最近发现ER Ca ~（2+）耗竭依赖的ER应激在骨骼肌分化中起生理作用。
Intracellular Ca2+ dynamics regulate various cellular functions. As the classic study by Ebashi reported, 1 skeletal muscle contraction is regulated by cytoplasmic Ca2+ released from the sarcoplasmic reticulum, which in turn activates troponin C. Since that discovery, Ca2+ action has drawn much attention in basic biomedical research because cytosolic Ca2+ can activate Ca2+-dependent proteins, and thereby modulate cellular activities and functions. However, recent studies have highlighted the significance of Ca2+ removal from the endoplasmic reticulum (ER).Increased cytosolic Ca2+ is caused by either Ca2+ release from calcium stores (eg, ER) or Ca2+ uptake from the extracellular space. When ER Ca2+ is released into the cytosol via ER Ca2+ channels, Ca2+ depletion occurs simultaneously in the ER. ER Ca2+ depletion is potentially harmful to cells, as it interferes with proper folding of proteins that are synthesized on the rough ER, because of dysfunction of ER Ca2+-dependent molecular chaperones (eg, calreticulin and calnexin). ER stress is a cellular condition in which misfolded proteins accumulate in the ER. 2 In addition to ER Ca2+ depletion, various other factors (eg, oxidative stress, glucose shortage, or heavy burden of protein synthesis) cause ER stress. 3 We have recently found that ER Ca2+ depletion-dependent ER stress plays a physiological role in skeletal muscle differentiation.