spondylitis/tyrosine

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Association Between Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22) Polymorphisms and Risk of Ankylosing Spondylitis: A Meta-analysis.

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BACKGROUND Ankylosing spondylitis (AS) is a chronic autoimmune disease that involves the imbalance of peripheral tolerance possibly caused by the negative signal of activated T cells. The polymorphisms in the human protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene have been pointed out

Lack of carboxyl-terminal tyrosine distinguishes the B2706-bound peptide repertoire from those of B2704 and other HLA-B27 subtypes associated with ankylosing spondylitis.

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B*2704 and B*2706 are two closely related HLA-B27 subtypes, which differ from the common B*2705 by the Asp > Ser77, Val > Glu152, and Ala > Gly211 amino acid changes. In addition, B*2706 differs from B*2704 by the His > Asp114 and Asp > Tyr116 changes. In spite of their similarity B*2704, but not

A functional variant of PTPN22 confers risk for Vogt-Koyanagi-Harada syndrome but not for ankylosing spondylitis.

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BACKGROUND Protein tyrosine phosphatase non-receptor 22 (PTPN22) is a key negative regulator of T lymphocytes and has emerged as an important candidate susceptibility factor for a number of immune-related diseases. This study aimed to examine the predisposition of PTPN22 SNPs to Vogt-Koyanagi-Harada

A variant within intron 1 of the PTPN22 gene decreases the genetic susceptibility of ankylosing spondylitis in a central south Chinese Han population.

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OBJECTIVE The protein tyrosine phosphatase non-receptor type 22 (PTPN22) is generally accepted as a key factor in maintaining immune cellular homeostasis. So far, no association has been reported between the polymorphisms of PTPN22 and ankylosing spondylitis (AS) in Chinese populations. We attempted

Plasma amino acid level in rheumatoid arthritis and ankylosing spondylitis and its variation during age.

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28 plasma amino acids of 40 female patients with rheumatoid arthritis (RA), 24 male patients with ankylosing spondylitis (ASp) and 19 controls (14 females and 5 males) were investigated. In RA-patients 19 amino acids showed statistically significant differences to healthy people of which 18 were

Suppression of Development of Ankylosing Spondylitis Through Soluble Flt-1.

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OBJECTIVE Circulating monocytes/macrophages are origins of osteoclasts that mediate the development of ankylosing spondylitis (AS). Moreover, infiltrated macrophages facilitate the AS progression through production and secretion of pro-inflammatory cytokines. Thus, suppression of the recruitment of

RNA Sequencing for Gene Expression Profiles in Peripheral Blood Mononuclear Cells with Ankylosing Spondylitis RNA

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Several previous studies have attempted to investigate the regulatory mechanisms underlying gene expression in ankylosing spondylitis (AS). However, the specific molecular pathways underlying this condition remain unclear. Previous research used next-generation RNA sequencing to identify a series of

Gene expression profiling analysis of patients with ankylosing spondylitis.

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METHODS A comprehensive bioinformatics analysis of genes which may have correlations with ankylosing spondylitis (AS). OBJECTIVE To study the mechanisms of AS by analyzing microarray of GSE25101. BACKGROUND AS is an inflammatory arthritis that can lead to chronic pain and

Up-regulation of fatty acid oxidation in the ligament as a contributing factor of ankylosing spondylitis: A comparative proteomic study.

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OBJECTIVE The present study first utilized a standardized shotgun proteomic analysis method to determine differences in protein expression of fibroblasts in the ligament between AS patients and healthy controls. METHODS Proteins extracted from primarily cultured FLLs from 35 AS patients and 10

Quantitative Proteomic Analysis of Peripheral Blood Mononuclear Cells in Ankylosing Spondylitis by iTRAQ.

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This study was designed to identify and quantify the different proteins expression levels in ankylosing spondylitis (AS) and to explore the pathogenesis of AS. We performed isobaric tags for relative and absolute quantitation (iTRAQ) coupled with multiple chromatographic fractionation and tandem

A proof-of-concept study with the tyrosine kinase inhibitor nilotinib in spondyloarthritis.

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To evaluate the immunomodulating and clinical effects of nilotinib, a tyrosine kinase inhibitor, in a proof-of-concept study in spondyloarthritis (SpA) assessing the mast cell as potential novel therapeutic target in this disease. Twenty eight patients with active peripheral (pSpA) and/or axial SpA

Protein tyrosine phosphatase nonreceptor type 2: an important regulator of lnterleukin-6 production in rheumatoid arthritis synovial fibroblasts.

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OBJECTIVE To investigate the role of protein tyrosine phosphatase nonreceptor type 2 (PTPN2) in the pathogenesis of rheumatoid arthritis (RA). METHODS Synovial tissue samples from patients with RA and patients with osteoarthritis (OA) were stained for PTPN2. Synovial fibroblasts were stimulated with

Associations of the PTPN22 and CTLA-4 genetic polymorphisms with Taiwanese ankylosing spondylitis.

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Ankylosing spondylitis (AS) is an autoimmune disease, and the imbalance of peripheral tolerance is involved in its pathogenesis. Importantly, the negative signal of activated T cells plays a crucial role in the balance of peripheral tolerance. It has been postulated that human protein tyrosine

Association of IL-12B genetic polymorphism with the susceptibility and disease severity of ankylosing spondylitis.

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OBJECTIVE Interleukin 23 (IL-23) stimulates the differentiation of T helper 17 (Th17) cells, which are involved in the pathogenesis of ankylosing spondylitis (AS). Binding of IL-23 to the IL-23 receptor complex activates Janus kinases 2 and tyrosine kinase 2, which phosphorylate IL-23R and

IL-17A induces osteoblast differentiation by activating JAK2/STAT3 in ankylosing spondylitis.

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BACKGROUND IL-17A has recently emerged as a potential target that regulates the extensive inflammation and abnormal bone formation observed in ankylosing spondylitis (AS). Blocking IL-17A is expected to inhibit bony ankylosis. Here, we investigated the effects of anti IL-17A agents in

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spondylitis/tyrosine

Association Between Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22) Polymorphisms and Risk of Ankylosing Spondylitis: A Meta-analysis.

Lack of carboxyl-terminal tyrosine distinguishes the B*2706-bound peptide repertoire from those of B*2704 and other HLA-B27 subtypes associated with ankylosing spondylitis.

A functional variant of PTPN22 confers risk for Vogt-Koyanagi-Harada syndrome but not for ankylosing spondylitis.

A variant within intron 1 of the PTPN22 gene decreases the genetic susceptibility of ankylosing spondylitis in a central south Chinese Han population.

Plasma amino acid level in rheumatoid arthritis and ankylosing spondylitis and its variation during age.

Suppression of Development of Ankylosing Spondylitis Through Soluble Flt-1.

RNA Sequencing for Gene Expression Profiles in Peripheral Blood Mononuclear Cells with Ankylosing Spondylitis RNA

Gene expression profiling analysis of patients with ankylosing spondylitis.

Up-regulation of fatty acid oxidation in the ligament as a contributing factor of ankylosing spondylitis: A comparative proteomic study.

Quantitative Proteomic Analysis of Peripheral Blood Mononuclear Cells in Ankylosing Spondylitis by iTRAQ.

A proof-of-concept study with the tyrosine kinase inhibitor nilotinib in spondyloarthritis.

Protein tyrosine phosphatase nonreceptor type 2: an important regulator of lnterleukin-6 production in rheumatoid arthritis synovial fibroblasts.

Associations of the PTPN22 and CTLA-4 genetic polymorphisms with Taiwanese ankylosing spondylitis.

Association of IL-12B genetic polymorphism with the susceptibility and disease severity of ankylosing spondylitis.

IL-17A induces osteoblast differentiation by activating JAK2/STAT3 in ankylosing spondylitis.

Baz done ki pi konplè remèd fèy medsin te apiye nan syans

Lack of carboxyl-terminal tyrosine distinguishes the B2706-bound peptide repertoire from those of B2704 and other HLA-B27 subtypes associated with ankylosing spondylitis.