The sigma-1 receptor: roles in neuronal plasticity and disease.

The sigma-1 receptor: roles in neuronal plasticity and disease.
复制标题

DOI:
10.1016/j.tins.2012.09.007
复制
发表时间:
2012-12
影响因子:
15.9
通讯作者:
Bonci A
Bonci A
中科院分区:
医学1区
文献类型:
--
作者:
Kourrich S;Su TP;Fujimoto M;Bonci A

文献摘要

参考文献

被引文献

相似文献

σ-1受体(Sig-1 Rs)与许多神经和精神疾病有关。Sig-1 R是一种细胞内伴侣蛋白,特异性地位于内质网(ER)-内质网蛋白界面(称为内质网蛋白相关ER膜(MAM))。在这里,Sig-1 Rs调节ER-β对Ca 2+信号的调节。在这篇综述中,我们讨论了目前对Sig-1 R功能的理解。基于此,我们认为,关键的细胞机制连接Sig-1 Rs的神经系统疾病涉及易位的Sig-1 Rs从MAM的其他部分的细胞,从而Sig-1 Rs结合和调节各种离子通道,受体,或激酶的活动。因此,Sig-1 Rs及其相关配体可能代表治疗神经和精神疾病某些方面的新途径。
Sigma-1 receptors (Sig-1Rs) have been implicated in many neurological and psychiatric conditions. The Sig-1R is an intracellular chaperone that resides specifically at the endoplasmic reticulum (ER)-mitochondrion interface referred to as the mitochondrion-associated ER membrane (MAM). Here, Sig-1Rs regulate ER-mitochondrion Ca2+ signaling. In this review, we discuss the current understanding of Sig-1R functions. Based on this, we suggest that the key cellular mechanism linking Sig-1Rs to neurological disorders involve the translocation of Sig-1Rs from the MAM to other parts of the cell, whereby Sig-1Rs bind and modulate the activities of various ion channels, receptors, or kinases. Thus, Sig-1Rs and their associated ligands may represent new avenues for treating some aspects of neurological and psychiatric diseases.
DOI: 10.1126/science.1166127
发表时间: 2009-02-13
期刊: Science (New York, N.Y.)
影响因子: --
作者:
Fontanilla D;Johannessen M;Hajipour AR;Cozzi NV;Jackson MB;Ruoho AE
通讯作者: Ruoho AE
DOI: 10.1007/978-90-481-8622-8_13
发表时间: 2010
影响因子: --
作者:
Hayashi, Teruo;Su, Tsung-Ping
通讯作者: Su, Tsung-Ping
DOI: 10.1016/j.neulet.2010.08.085
发表时间: 2010-12-10
影响因子: 2.5
作者:
Catterall WA
通讯作者: Catterall WA
DOI: 10.1016/j.pharmthera.2010.04.003
发表时间: 2010-09
影响因子: 13.5
作者:
Fishback, James A.;Robson, Matthew J.;Xu, Yan-Tong;Matsumoto, Rae R.
通讯作者: Matsumoto, Rae R.
靶向配体的伴侣伴侣Sigma-1受体在神经精神疾病的治疗中。
DOI: 10.1517/14728222.2011.560837
发表时间: 2011-05
影响因子: 5.8
作者:
Hayashi T;Tsai SY;Mori T;Fujimoto M;Su TP
通讯作者: Su TP