The Relationship Between Protein S-Nitrosylation and Human Diseases: A Review
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REVIEW
The Relationship Between Protein S‑Nitrosylation and Human Diseases: A Review Yadi Zhang1,2 · Yuzhen Deng1,2 · Xiaoxi Yang1,2 · Hongmei Xue1,2 · Yumiao Lang1,2 Received: 10 July 2020 / Revised: 18 August 2020 / Accepted: 19 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract S-nitrosylation (SNO) is a covalent post-translational oxidative modification. The reaction is the nitroso group (–NO) to a reactive cysteine thiol within a protein to form the SNO. In recent years, a variety of proteins in human body have been found to undergo thiol nitrosylation under specific conditions. Protein SNO, which is closely related to cardiovascular disease, Parkinson’s syndrome, Alzheimer’s disease and tumors, plays an important role in regulatory mechanism of protein function in both physiological and pathological pathways, such as in cellular homeostasis and metabolism. This review discusses possible molecular mechanisms protein SNO modification, such as the role of NO in vivo and the formation mechanism of SNO, with particular emphasis on mechanisms utilized by SNO to cause certain diseases of human. Importantly, the effect of SNO on diseases is multifaceted and multi-channel, and its critical value in vivo is not well defined. Intracellular redox environment is also a key factor affecting its level. Therefore, we should pay more attention to the equilibrium relationship between SNO and denitrosylation pathway in the future researches. These findings provide theoretical support for the improvement or treatment of diseases from the point of view of SNO. Keywords Nitric oxide · S-nitrosylation · Denitrosylation · Human diseases · Mechanism
Introduction Protein S-nitrosylation (SNO), the nitric oxide mediated redox-type reversible modification of cysteine thiols, exists in proteins in virtually all biological systems and affects protein activity, protein–protein interactions and protein localization [1]. NO induced SNO plays a significant role in the regulation of cellular signal transduction. Previous studies have demonstrated that SNO is possibly involved in regulating apoptosis [2], muscle contraction [3], and protein homeostasis [4]. For example, the differentiation of cardiomyocytes can be promoted by nitrosylated of Prdx-2 [5].
* Yumiao Lang [email protected] 1
Key Laboratory of Public Health Safety of Hebei Province, College of Public Health, Hebei University, No. 180 Wusidong Road, Baoding 071002, People’s Republic of China
Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of Ministry of Education, Institute of Life Science and Green Development, Hebei University, Baoding 071002, People’s Republic of China
2
Thiol nitrosylation of NF-kB p50 can regulate its DNA binding activity [6]. Nitrosylation of p35-Cys92 mediates Cdk5 activity and promotes synaptic formation of neurons [7]. In addition, nitrosylated proteins can also be denitrosylated under the action of certain enzymes. Similarly, denitrosylation can also have an impact on disease. For example,
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