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神经元中钙离子进入的加速器与刹车
作者:小柯机器人 发布时间:2024/9/13 19:10:01

俄罗斯科学院Elena Kaznacheyeva团队综述了STIM蛋白——神经元中钙离子进入的加速器与刹车。2024年9月12日,《神经科学通报》杂志在线发表了这项成果。

研究人员表示,基质相互作用分子(STIM)是内质网中Ca2+储存库的Ca2+传感器。它们激活库操作型Ca2+通道,这些通道是非兴奋性细胞中Ca2+进入的主要来源。此外,STIM蛋白还与其他Ca2+通道亚基和主动转运蛋白相互作用,使其成为调控各种Ca2+流入兴奋性细胞的重要中间分子。

然而,关于STIM蛋白在大脑功能中的作用知之甚少。STIM蛋白参与多种信号通路,负责补充神经元内的Ca2+储存,并介导突触传递和神经元的兴奋性。Ca2+失衡是许多脑部病理状态的标志,包括神经退行性疾病、损伤、中风和癫痫。STIM蛋白在这些病变中发挥作用,不仅通过支持异常的库操作型Ca2+进入,还通过调控其他通道的Ca2+流入。

研究人员综述了当前关于STIM蛋白在神经元中的研究现状及其在脑病理中的参与。

附:英文原文

Title: STIM Proteins: The Gas and Brake of Calcium Entry in Neurons

Author: Skobeleva, Ksenia, Wang, Guanghui, Kaznacheyeva, Elena

Issue&Volume: 2024-09-12

Abstract: Stromal interaction molecules (STIM)s are Ca2+ sensors in internal Ca2+ stores of the endoplasmic reticulum. They activate the store-operated Ca2+ channels, which are the main source of Ca2+ entry in non-excitable cells. Moreover, STIM proteins interact with other Ca2+ channel subunits and active transporters, making STIMs an important intermediate molecule in orchestrating a wide variety of Ca2+ influxes into excitable cells. Nevertheless, little is known about the role of STIM proteins in brain functioning. Being involved in many signaling pathways, STIMs replenish internal Ca2+ stores in neurons and mediate synaptic transmission and neuronal excitability. Ca2+ dyshomeostasis is a signature of many pathological conditions of the brain, including neurodegenerative diseases, injuries, stroke, and epilepsy. STIMs play a role in these disturbances not only by supporting abnormal store-operated Ca2+ entry but also by regulating Ca2+ influx through other channels. Here, we review the present knowledge of STIMs in neurons and their involvement in brain pathology.

DOI: 10.1007/s12264-024-01272-5

Source: https://link.springer.com/article/10.1007/s12264-024-01272-5

期刊信息

Neuroscience Bulletin《神经科学通报》,创刊于2006年。隶属于施普林格·自然出版集团,最新IF:5.6

官方网址:https://link.springer.com/journal/12264
投稿链接:https://mc03.manuscriptcentral.com/nsb