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使用光激活蛋白激酶进行MKK6和p38信号的剖析

Shah Md Toufiqur Rahman¹, Wenyuan Zhou², Alexander Deiters²

¹Department of Chemical and Biomolecular Engineering, North Carolina State University, Campus Box 7905, 911 Partners Way, Raleigh, NC, 27695, USA.

Chembiochem : a European journal of chemical biology

|October 19, 2023

概括

光遗传学使得精确研究压力激活蛋白激酶 (SAPKs) 成为可能. 光激活的p38α和MKK6迅速触发了细胞亡并抑制了细胞生存途径,澄清了它们在细胞命运中的作用.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
信号通道的信号通道

背景情况:

压力激活的信号通路对于细胞反应至关重要.
研究压力激活蛋白激酶 (SAPKs) 是困难的,因为在压力下细胞适应和选择压力.
光遗传学提供了一种新的方法来精确控制和研究这些途径.

研究的目的:

通过光遗传系统研究p38α及其上游激活剂MKK6在压力诱导的细胞反应中的作用.
阐明p38α和MKK6激活对细胞亡和细胞存活机制的动力学和下游影响.
为了澄清p38α,MKK6和ERK信号通路之间的相互作用.

主要方法:

开发和应用单等离子体光遗传系统来表达光激活的p38α或MKK6.
使用活细胞光显微镜来监测饥饿细胞中的信号事件.
通过短暂的紫外线照射 (衰老) 诱导p38α或MKK6的激活.

主要成果:

光诱导的p38α或MKK6激活迅速启动了p38介导的信号传递,细胞染色体c的释放和具有明显动态的亡.
激活p38α抑制了自细胞形成,模仿生长因子诱导的PI3K/Akt/mTORC1信号传递.
活性MKK6抑制了血清诱导的ERK活性,激活的p38α阻断了饥饿细胞中生长因子刺激的ERK信号传递.

结论:

光遗传系统为SAPK激活提供了精确的时间控制,克服了传统应激诱导的挑战.
p38α和MKK6在调节亡中起着至关重要的作用,同时抑制自和ERK信号传递等支持生存的途径.
这些发现提供了更清晰的理解动态信号网络,控制在压力下细胞命运决策.

关键词:

灭症 (apoptosis) 是一种死亡的过程.自自是自的过程.细胞死亡是细胞死亡.增长因素增长因素增长因素通过基因激活的蛋白质激酶.视觉遗传学视觉遗传学信号传导的信号传导.

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