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Updated: May 24, 2025

Novel RNA-Binding Proteins Isolation by the RaPID Methodology
Published on: September 30, 2016
Identification of PTPRC as a potential serum biomarker in rheumatoid arthritis using bioinformatics analysis and
Yongwang Hou1, Zhichao Yang2, Junshuai Ma1
1Clinical Laboratory, The First Affiliated Hospital of Hebei North University, Zhangjiakou City, Hebei Province 075000, China.
Background:
Rheumatoid arthritis (RA) is a multifactorial autoimmune disease affecting joints. Early and accurate diagnosis is important for initiating the correct treatment and preventing long-term complications.
Methods:
Microarray expression data of synovial tissues from people with osteoarthritis and healthy populations were downloaded from the Gene Expression Omnibus (GEO) database. Extracellular protein-differentially expressed genes (EP-DEGs) were screened using protein annotation databases. GO and KEGG were used to analyze the function and pathway of EP-DEGs. STRING, Cytoscape, and CytoHubba were used to construct a protein-protein interaction (PPI) network and screen key EP-DEGs. Serum PTPRC levels were measured by ELISA. Molecular docking was used to explore the affinity of drugs for PTPRC.
Results:
A total of 135 potential target genes of EP-DEGs in RA were identified using Venn analysis. The EP-DEGs were enriched in the B cell receptor signaling pathway, humoral immune response, cytokine-cytokine receptor interaction, chemokine signaling pathway and PI3K-Akt signaling pathway. PTPRC was identified as a hub gene and its expression in RA was high. The ROC curve of PTPRC concentration in RA was plotted to obtain an AUC of 0.9191, a cutoff value of 39.38 pg/mL, and a sensitivity and specificity of 77.05 % and 73.33 %, respectively. Molecular docking analysis showed that prednisone, methotrexate, dexamethasone and cyclophosphamide bound to PTPRC with Vina scores of -9.2, -8.7, -10.1, and - 5.1, respectively.
Conclusion:
PTPRC may be a potential marker for the diagnosis and a potential target for the treatment of RA and the mechanism of PTPRC involvement in RA may regulate immune function through PI3K-Akt signaling pathway.
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