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Differential Expression Study of Lysine Crotonylation and Proteome for Chronic Obstructive Pulmonary Disease Combined with Type II Respiratory Failure
Author(s) -
Qing Gan,
Donge Tang,
Qiang Yan,
Jiejing Chen,
Yong Xu,
Wen Xue,
Lu Xiao,
Fengping Zheng,
Huixuan Xu,
Yingyun Fu,
Yong Dai
Publication year - 2021
Publication title -
canadian respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.675
H-Index - 53
eISSN - 1916-7245
pISSN - 1198-2241
DOI - 10.1155/2021/6652297
Subject(s) - kegg , proteome , copd , downregulation and upregulation , histone , medicine , lysine , gene expression , gene , biology , bioinformatics , biochemistry , transcriptome , amino acid
The modification of lysine crotonylation (Kcr) is another biological function of histone in addition to modification of lysine acetylation (Kac), which may play a specific regulatory role in diseases.Objectives This study compared the expression levels of Kcr and proteome between patients with chronic obstructive pulmonary disease (COPD) combined with type II respiratory failure (RF) to study the relationship between Kcr, proteome, and COPD.Methods We tested the Kcr and proteome of COPD combined with type II RF and normal control (NC) using croton acylation enrichment technology and liquid chromatography tandem mass spectrometry (LC-MS/MS) with high resolution.Results We found that 32 sites of 23 proteins were upregulated and 914 sites of 295 proteins were downregulated. We performed Kyoto Encyclopedia of Genes and Genomes (KEGG), protein domain, and Gene Ontology (GO) analysis on crotonylated protein. In proteomics research, we found that 190 proteins were upregulated and 151 proteins were downregulated. Among them, 90 proteins were both modified by differentially expressed crotonylation sites and differentially expressed in COPD combined with type II RF and NC.Conclusion Differentially expressed crotonylation sites may be involved in the development of COPD combined with type II RF. 90 proteins modified by crotonylation and differentially expressed in COPD combined with type II RF can be used as markers for the study of the molecular pathogenesis of COPD combined with type II RF.

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