细胞质磷脂酶A2与力学信号转导  

Cytoplasmic phospholipase A2 and mechanical signal transduction

在线阅读下载全文

作  者:樊林玮 周菁 FAN Linwei;ZHOU Jing(Department of Physiology and Pathophysiology,School of Basic Medical Sciences,Peking University,National Key Laboratory of Vascular Homeostasis and Remodeling,Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides,National Health Commission,Beijing Key Laboratory of Cardiovascular Receptors Research,Beijing 100191,China)

机构地区:[1]北京大学基础医学院,生理学与病理生理学系,血管稳态与重构全国重点实验室,国家卫生健康委员会心血管分子生物学与调节肽重点实验室,心血管受体研究北京市重点实验室,北京100191

出  处:《生命的化学》2023年第7期959-966,共8页Chemistry of Life

基  金:国家自然科学基金面上项目(82270419)。

摘  要:细胞拥有感知周围微环境的能力,细胞的行为与微环境有密切的关系,但是微环境影响细胞行为的机制未被探明。近年来,很多研究提出,细胞的这种感知能力很大部分来自于细胞核。本文介绍了一种新发现的细胞核的力学传感器——细胞质磷脂酶A2(cPLA2)的力学信号转导功能。它能够感受不同类型的力学刺激,通过易位到核膜上,激活下游不同信号通路从而调控细胞功能。对cPLA2的深入认识将为进一步探索细胞核的力学信号感知功能提供新的思路。Cells possess the remarkable capacity to assess and interpret their surrounding microenvironment.The behavior of cells is intimately intertwined with the influence exerted by this microenvironment.However,the precise mechanisms through which various environmental factors impact cells remain largely unknown.In recent years,numerous investigations have postulated that the nucleus plays a pivotal role in its perceptual capabilities.This paper reviews the functional role of a recently identified nuclear mechanical sensor known as cytoplasmic phospholipase A2(cPLA2).Remarkably,cPLA2 exhibits the ability to detect diverse forms of mechanical stimuli,is capable of translocating to the nuclear membrane,and subsequently activates distinct downstream signaling pathways,thereby modulating various cellular functions.A comprehensive understanding of cPLA2 paves the way for novel avenues of exploration into the nucleus'ability to perceive mechanical signals.

关 键 词:细胞质磷脂酶A2 细胞力学微环境 力学传感器 核膜张力 

分 类 号:R318.01[医药卫生—生物医学工程]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象