ArticleScientific reports2017
Protein tyrosine phosphatase non-receptor 22 and C-Src tyrosine kinase genes are down-regulated in patients with rheumatoid arthritis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Article
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- Selection signatures for local and regional adaptation in Chinese Mongolian horse breeds reveal candidate genes for hoof health.BMC genomics · 2023Article
- Platelets-related signature based diagnostic model in rheumatoid arthritis using WGCNA and machine learning.Frontiers in immunology · 2023Article
- Expression and function analysis of microRNA in collagen-induced arthritis rats.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Genetic Polymorphism ofMedicina (Kaunas, Lithuania) · 2022Review
- A reference catalog of DNA palindromes in the human genome and their variations in 1000 Genomes.Human genome variation · 2020Article
- Non-receptor tyrosine kinase signaling in autoimmunity and therapeutic implications.Pharmacology & therapeutics · 2019Review
- The Contribution of PTPN22 to Rheumatic Disease.Arthritis & rheumatology (Hoboken, N.J.) · 2019Review
- Methods and approaches to disease mechanisms using systems kinomics.Synthetic and systems biotechnology · 2018Review
- Accelerating annotation of articles via automated approaches: evaluation of the neXtA5 curation-support tool by neXtProt.Database : the journal of biological databases and curation · 2018Article
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Authors and funding
17 authors at 5 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Several protein tyrosine phosphatase non-receptor 22 (PTPN22) single-nucleotide polymorphisms (SNPs) have been significantly related with rheumatoid arthritis (RA) susceptibility. Nevertheless, its potential influence on PTPN22 expression in RA has not been completely elucidated. Furthermore, PTPN22 binds to C-Src tyrosine kinase (CSK) forming a key complex in autoimmunity. However, the information of CSK gene in RA is scarce. In this study, we analyzed the relative PTPN22 and CSK expression in peripheral blood from 89 RA patients and 43 controls to determine if the most relevant PTPN22 (rs2488457, rs2476601 and rs33996649) and CSK (rs34933034 and rs1378942) polymorphisms may influence on PTPN22 and CSK expression in RA. The association between PTPN22 and CSK expression in RA patients and their clinical characteristics was also evaluated. Our study shows for the first time a marked down-regulation of PTPN22 expression in RA patients carrying the risk alleles of PTPN22 rs2488457 and rs2476601 compared to controls (p = 0.004 and p = 0.007, respectively). Furthermore, CSK expression was significantly lower in RA patients than in controls (p < 0.0001). Interestingly, a reduced PTPN22 expression was disclosed in RA patients with ischemic heart disease (p = 0.009). The transcriptional suppression of this PTPN22/CSK complex may have a noteworthy clinical relevance in RA patients.
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