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• W4379469135 abstract "Vitiligo is an acquired depigmented skin disorder. Though genetic background, autoimmune dysregulation, and oxidative stress were reported involved in the development of vitiligo, the exact pathogenesis remains largely unknown. This study aimed to investigate potential functional proteins, pathways, and serum biomarkers involved in active vitiligo.Tandem Mass Tags (TMT) method was used to determine differentially expressed proteins (DEPs) in serum samples between 11 active vitiligo patients and 7 healthy controls of Chinese Han population.A total of 31 DEPs were identified (P < 0.05, fold change >1.2), with 21 proteins upregulated and 10 proteins downregulated in the vitiligo group. DEPs were enriched in GO terms such as extracellular exosome and immunoglobulin receptor binding, as well as KEGG pathways including cysteine and methionine metabolism and other immune-related pathways. Furthermore, ALDH1A1 and EEF1G achieved areas under receiver-operating characteristic (ROC) curve of 0.9221 and 0.8571, respectively. The expression levels of these 2 proteins were validated in another active vitiligo patient group.Our research provided novel insight into serum proteomic profile for vitiligo patients, detecting ALDH1A1 and EEF1G as potential biomarkers for active vitiligo and therapeutic intervention. Our work also detected several DEPs and associated pathways in the serum of active vitiligo patients, reinforcing the roles of retinoic acid and exosome processes in vitiligo pathogenesis." @default.
• W4379469135 created "2023-06-07" @default.
• W4379469135 creator A5029705815 @default.
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• W4379469135 date "2023-06-01" @default.
• W4379469135 modified "2023-09-25" @default.
• W4379469135 title "TMT-Based Quantitative Proteomic and Physiological Analyses on Serums of Chinese Patients with Active Vitiligo" @default.
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• W4379469135 doi "https://doi.org/10.2147/ccid.s412124" @default.
• W4379469135 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37303983" @default.
• W4379469135 hasPublicationYear "2023" @default.
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