myasthenia gravis/phosphatase

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Decreased expression of Src homology 2 domain-containing protein tyrosine phosphatase 1 reduces T cell activation threshold but not the severity of experimental autoimmune myasthenia gravis.

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Myasthenia gravis (MG) and its murine model experimental autoimmune myasthenia gravis (EAMG) are T cell-dependent, antibody-mediated autoimmune diseases. Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1) is a cytosolic tyrosine phosphatase that is involved in regulating the T

Anti-alkaline phosphatase antibody positive myasthenia gravis.

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Anti-alkaline phosphatase antibody (AP Ab) was specific in 9% of 249 anti-acetylcholine receptor (AChR) Ab-positive myasthenia gravis (MG) (SPMG) patients but not in patients with AChR Ab-negative MG (SNMG), other neurological and immunological diseases, or healthy volunteers. No cross-reactivity

Gravin, an autoantigen recognized by serum from myasthenia gravis patients, is a kinase scaffold protein.

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BACKGROUND Subcellular targeting of protein kinases and phosphatases provides a mechanism for co-localizing these enzymes with their preferred substrates. A recently identified mammalian scaffold protein, AKAP79, controls the location of two broad-specificity kinases and a phosphatase. RESULTS We

Genetic factors in autoimmune myasthenia gravis.

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Autoimmune myasthenia gravis (MG) is a multifactorial disease, markedly influenced by genetic factors, even though it shows limited heritability. The clinically typical form of autoimmune MG with thymus hyperplasia shows the most reproducible genetic associations, especially with the A1-B8-DR3 (8.1)

SHP2 inhibitor protects AChRs from effects of myasthenia gravis MuSK antibody.

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To determine whether an SRC homology 2 domain-containing phosphotyrosine phosphatase 2 (SHP2) inhibitor would increase muscle-specific kinase (MuSK) phosphorylation and override the inhibitory effect of MuSK-antibodies (Abs).The effect of the SHP2 inhibitor

Generalized trichoepitheliomas with alopecia and myasthenia gravis: clinicopathologic and immunohistochemical study and comparison with classic and desmoplastic trichoepithelioma.

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We report on a patient with a syndrome characterized by smooth facial papules and nodules; alopecia of the eyebrows, eyelashes, and most body hair; mild alopecia of scalp hair; possibly hypohidrosis; and myasthenia gravis. The clinical, histologic, and immunohistochemical findings are compared with

Expression and clinical significance of protein tyrosine phosphatase nonreceptor 22 in resected thymoma.

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BACKGROUND To investigate the expression and clinical significance of protein tyrosine phosphatase nonreceptor 22 (PTPN22) in thymoma, as well as the relationship between thymoma and myasthenia gravis (MG). METHODS The expression of PTPN22 in normal thymus (35 cases), thymoma without MG (50 cases),

The autoimmunity-related polymorphism PTPN22 1858C/T is associated with anti-titin antibody-positive myasthenia gravis.

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Genetic variation in the intracellular tyrosine phosphatase PTPN22 has been recently associated with susceptibility to various autoimmune diseases. Myasthenia gravis (MG) is a complex genetic disease with a distinct clinical and pathological heterogeneity. We conducted a case-control association

The association of PTPN22 R620W polymorphism is stronger with late-onset AChR-myasthenia gravis in Turkey.

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A functional single nucleotide polymorphism (SNP) of the PTPN22 gene encoding a protein tyrosine phosphatase has been associated with autoimmune disorders including myasthenia gravis (MG). As the PTPN22 R620W polymorphism has a wide variation of allele frequencies among different populations, this

Gene Polymorphisms for Both Auto-antigen and Immune-Modulating Proteins Are Associated with the Susceptibility of Autoimmune Myasthenia Gravis.

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Myasthenia gravis (MG) is an antibody-mediated autoimmune disease against antigens at the neuromuscular junction. Both genetic and environmental factors contribute to the susceptibility of MG. We undertook a case-control study to explore the contribution of genes of the auto-antigen and

Double labelled T suppressor lymphocytes in the thymus of a patient with myasthenia gravis: morphological and immunological characteristics.

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Double labelled lymphocytes were prevalent in the thymus of a 32-year-old woman with myasthenia gravis. The simultaneous presence of both E and C3b surface receptors was demonstrated. Focal paranuclear acid phosphatase activity of the cells supported their T cell origin. Histological analysis

Detection of the phosphatase activity of carbonic anhydrase III on a nitrocellulose membrane following 2D gel electrophoresis.

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Carbonic anhydrase isozyme III (CAIII) is unique among the carbonic anhydrases because it exhibits phosphatase activity. CAIII is relatively specific to skeletal muscles, and may therefore be a useful diagnostic marker for muscular diseases. In the muscles of patients with myasthenia gravis (MG),

PTPN22 and CTLA-4 gene polymorphisms in resected thymomas and thymus for myasthenia gravis.

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Myasthenia gravis (MG) is an autoimmune disease of striated muscle tissue mediated by autoantibodies. MG is often treated with thymectomy. Protein tyrosine phosphatase non-receptor 22 (PTPN22) and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) have recently been found to be the genes that

Macromolecular alkaline phosphatase and an immunoglobulin G that inhibited alkaline phosphatase in a patient's serum.

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Macromolecular alkaline phosphatase (EC 3.1.3.1) was found in the serum of a patient suffering from myasthenia gravis (adult type II) complicated with thymoma, and was shown by immunoelectrophoresis to be bound to immunoglobulins A and G (IgG). Placental alkaline phosphatase, complexed with either

The PTPN22gain-of-function+1858T(+) genotypes correlate with low IL-2 expression in thymomas and predispose to myasthenia gravis.

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Protein tyrosine phosphatase, non-receptor type 22 (PTPN22) inhibits T-cell activation and interleukin-2 (IL-2) production. The PTPN22(gain-of-function)+1858T(+) genotypes predispose to multiple autoimmune diseases, including early-onset (non-thymomatous) myasthenia gravis (MG). The disease

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