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本文引用的文献

1
S-nitrosylation of beta-catenin by eNOS-derived NO promotes VEGF-induced endothelial cell permeability.内皮型一氧化氮合酶(eNOS)产生的一氧化氮(NO)导致β-连环蛋白的 S-亚硝基化,促进血管内皮生长因子(VEGF)诱导的血管内皮细胞通透性增加。
Mol Cell. 2010 Aug 13;39(3):468-76. doi: 10.1016/j.molcel.2010.07.013.
2
Estradiol-17beta stimulates specific receptor and endogenous nitric oxide-dependent dynamic endothelial protein S-nitrosylation: analysis of endothelial nitrosyl-proteome.雌二醇-17β刺激特异性受体和内源性一氧化氮依赖的动态内皮蛋白 S-亚硝酰化:内皮一氧化氮蛋白组分析。
Endocrinology. 2010 Aug;151(8):3874-87. doi: 10.1210/en.2009-1356. Epub 2010 Jun 2.
3
17beta-Estradiol induces protein S-nitrosylation in the endothelium.17β-雌二醇诱导内皮细胞蛋白质 S-亚硝基化。
Cardiovasc Res. 2010 Mar 1;85(4):796-805. doi: 10.1093/cvr/cvp368. Epub 2009 Nov 13.
4
Role of local production of endothelium-derived nitric oxide on cGMP signaling and S-nitrosylation.内皮源性一氧化氮的局部产生在 cGMP 信号转导和 S-亚硝基化中的作用。
Am J Physiol Heart Circ Physiol. 2010 Jan;298(1):H112-8. doi: 10.1152/ajpheart.00614.2009. Epub 2009 Oct 23.
5
Protein denitrosylation: enzymatic mechanisms and cellular functions.蛋白质去亚硝基化:酶促机制与细胞功能
Nat Rev Mol Cell Biol. 2009 Oct;10(10):721-32. doi: 10.1038/nrm2764. Epub 2009 Sep 9.
6
Shear flow increases S-nitrosylation of proteins in endothelial cells.剪切流增加内皮细胞中蛋白质的S-亚硝基化。
Cardiovasc Res. 2009 Aug 1;83(3):536-46. doi: 10.1093/cvr/cvp154. Epub 2009 May 15.
7
Endogenous S-nitrosothiols protect against myocardial injury.内源性S-亚硝基硫醇可预防心肌损伤。
Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6297-302. doi: 10.1073/pnas.0901043106. Epub 2009 Mar 26.
8
SDF-1alpha stimulates JNK3 activity via eNOS-dependent nitrosylation of MKP7 to enhance endothelial migration.基质细胞衍生因子-1α通过内皮型一氧化氮合酶依赖的丝裂原活化蛋白激酶磷酸酶7亚硝基化刺激JNK3活性,以增强内皮细胞迁移。
Proc Natl Acad Sci U S A. 2009 Apr 7;106(14):5675-80. doi: 10.1073/pnas.0809568106. Epub 2009 Mar 23.
9
Acute hypoxia enhances proteins' S-nitrosylation in endothelial cells.急性低氧增强内皮细胞中蛋白质的S-亚硝基化。
Biochem Biophys Res Commun. 2008 Dec 26;377(4):1274-8. doi: 10.1016/j.bbrc.2008.10.144. Epub 2008 Nov 6.
10
S-nitrosylation of beta-arrestin regulates beta-adrenergic receptor trafficking.β-抑制蛋白的S-亚硝基化调节β-肾上腺素能受体的转运。
Mol Cell. 2008 Aug 8;31(3):395-405. doi: 10.1016/j.molcel.2008.05.024.

蛋白质的 S-亚硝基化:eNOS 衍生的 NO 调节内皮细胞功能的新见解。

S-nitrosylation of proteins: a new insight into endothelial cell function regulated by eNOS-derived NO.

机构信息

Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.

出版信息

Nitric Oxide. 2011 Aug 1;25(2):95-101. doi: 10.1016/j.niox.2011.04.014. Epub 2011 Apr 30.

DOI:10.1016/j.niox.2011.04.014
PMID:21554971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3152628/
Abstract

Nitric oxide (NO) is a messenger molecule that is highly diffusible and short-lived. Despite these two characteristics, seemingly unsuitable for intracellular reactions, NO modulates a variety of cellular processes via the mechanism of S-nitrosylation. An important factor that determines the specificity of S-nitrosylation as a signaling mechanism is the compartmentalization of nitric oxide synthase (NOS) with its target proteins. Endothelial NOS (eNOS) is unique among the NOS family members by being localized mainly near specific intracellular membrane domains including the cytoplasmic face of the Golgi apparatus and plasma membrane caveolae. Nitric oxide produced by eNOS localized on the Golgi apparatus can react with thiol groups on nearby Golgi proteins via a redox mechanism resulting in S-nitrosylation of these proteins. This modification influences their function as regulators of cellular processes such as protein trafficking (e.g., exocytosis and endocytosis), redox state, and cell cycle. Thus, eNOS-derived NO regulates a wide range of endothelial cell functions, such as inflammation, apoptosis, permeability, migration, and cell growth.

摘要

一氧化氮(NO)是一种信使分子,具有高度的扩散性和短暂的寿命。尽管有这两个特点,NO 似乎不适合细胞内反应,但它通过 S-亚硝基化的机制调节多种细胞过程。决定 S-亚硝基化作为信号机制特异性的一个重要因素是一氧化氮合酶(NOS)与其靶蛋白的区室化。内皮型一氧化氮合酶(eNOS)在 NOS 家族成员中是独特的,主要定位于包括高尔基器细胞质面和质膜小窝在内的特定细胞内膜域。定位于高尔基器上的 eNOS 产生的一氧化氮可以通过氧化还原机制与附近高尔基蛋白上的巯基反应,导致这些蛋白质的 S-亚硝基化。这种修饰影响它们作为细胞过程调节剂的功能,如蛋白质运输(例如,胞吐和胞吞)、氧化还原状态和细胞周期。因此,eNOS 衍生的 NO 调节广泛的内皮细胞功能,如炎症、细胞凋亡、通透性、迁移和细胞生长。