Emerging role of protein modification in inflammatory bowel disease.

Gaoying Wang; Jintao Yuan; Ji Luo; Dickson Kofi Wiredu Ocansey; Xu Zhang; Hui Qian; Wenrong XU; Fei Mao

Return

Emerging role of protein modification in inflammatory bowel disease.

Author: Gaoying WANG ¹ ; Jintao YUAN ² ; Ji LUO ¹ ; Dickson Kofi Wiredu OCANSEY ¹ ; Xu ZHANG ¹ ; Hui QIAN ¹ ; Wenrong XU ¹ ; Fei MAO ³
Author Information

1. Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University, Zhenjiang 212013, China.
2. Clinical Laboratory, the People's Hospital of Danyang, Affiliated Danyang Hospital of Nantong University, Zhenjiang 212300, China.
3. Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University, Zhenjiang 212013, China. maofei2003@ujs.edu.cn.
Publication Type:Review
Keywords: Acetylation; Glycosylation; Inflammatory bowel disease (IBD); Neddylation; Protein modification; Sumoylation
MeSH: Cytokines/genetics*; Humans; Inflammatory Bowel Diseases; NF-kappa B/metabolism*; Protein Processing, Post-Translational; Tumor Necrosis Factor-alpha/metabolism*
From: Journal of Zhejiang University. Science. B 2022;23(3):173-188
CountryChina
Language:English
Abstract: The onset of inflammatory bowel disease (IBD) involves many factors, including environmental parameters, microorganisms, and the immune system. Although research on IBD continues to expand, the specific pathogenesis mechanism is still unclear. Protein modification refers to chemical modification after protein biosynthesis, also known as post-translational modification (PTM), which causes changes in the properties and functions of proteins. Since proteins can be modified in different ways, such as acetylation, methylation, and phosphorylation, the functions of proteins in different modified states will also be different. Transitions between different states of protein or changes in modification sites can regulate protein properties and functions. Such modifications like neddylation, sumoylation, glycosylation, and acetylation can activate or inhibit various signaling pathways (e.g., nuclear factor-‍κB (NF-‍κB), extracellular signal-regulated kinase (ERK), and protein kinase B (AKT)) by changing the intestinal flora, regulating immune cells, modulating the release of cytokines such as interleukin-1β (IL-‍‍1β), tumor necrosis factor-α (TNF‍-‍α), and interferon-‍γ (IFN-‍γ), and ultimately leading to the maintenance of the stability of the intestinal epithelial barrier. In this review, we focus on the current understanding of PTM and describe its regulatory role in the pathogenesis of IBD.