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免疫细胞的S-亚硝基化/去亚硝基化与细胞凋亡

S-nitrosylation/denitrosylation and apoptosis of immune cells.

作者信息

Duan Shaojin, Chen Chang

机构信息

Guang An Men Hospital, China Academy of Chinese Medical Sciences, Beijing 10053, China.

出版信息

Cell Mol Immunol. 2007 Oct;4(5):353-8.

Abstract

Nitric oxide (NO) as an immunoregulatory molecule, predominantly depending on S-nitrosylation, acts as a versatile player that executes its regulation and signal transduction for exerting its multi-functions and pleiotropy. Apoptosis of immune cells is an intricate process coupled with positive/negative selection depending on integrated diverse endogenous and exogenous signals and functions to sustain homeostasis in the immune system. Here, the dual roles of NO depending on its concentration in apoptosis are reviewed, breeding up a switch mode in the apoptotic process. Following comments of different switches from apoptosis-death, a new finding of checkpoint (early fluorescence point) of GSNO-initiated thymocyte apoptosis and NOS-GSNOR double control are highlighted. Moreover, S-nitrosylation/denitrosylation, being as a redox switch, logically approaches to networks of metabolism itself and further accesses the neuroendicrine-immune-free radical network as a whole. Moreover, the host defense mediated by NO on pathogens, via protein S-nitrosylation are also discussed.

摘要

一氧化氮(NO)作为一种免疫调节分子,主要依赖于S-亚硝基化,是一个多功能的参与者,通过执行其调节和信号转导来发挥其多种功能和多效性。免疫细胞的凋亡是一个复杂的过程,它依赖于整合多种内源性和外源性信号进行正/负选择,并在免疫系统中维持内环境稳定。在此,我们综述了NO根据其浓度在凋亡中的双重作用,提出了凋亡过程中的一种转换模式。在评论了从凋亡到死亡的不同转换之后,重点介绍了GSNO引发的胸腺细胞凋亡的新发现——检查点(早期荧光点)以及NOS-GSNOR双重控制。此外,S-亚硝基化/去亚硝基化作为一种氧化还原开关,从逻辑上与代谢自身网络相关,并进一步作为一个整体进入神经内分泌-免疫自由基网络。此外,还讨论了NO通过蛋白质S-亚硝基化对病原体介导的宿主防御作用。

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