Human Receptor III for the Fc region of immunoglobulin G (FcGRIII) ELISA Kit

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AE63095HU
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Product Name Human Receptor III for the Fc region of immunoglobulin G (FcGRIII) ELISA Kit
Description Aitman et al. showed that copy number variation of the orthologous rat and human Fcgr3 genes is a determinant of susceptibility to immunologically mediated glomerulonephritis. Positional cloning identified loss of the rat-specific Fcgr3 paralog 'Fcgr3-related sequence' (Fcgr3rs) as a determinant of macrophage overactivity and glomerulonephritis in Wistar Kyoto rats. In humans, low copy number of FCGR3B, an ortholog of rat Fcgr3, was associated with glomerulonephritis in the autoimmune disorder systemic lupus erythematosus (SLE. Aitman et al. concluded that their finding that gene copy number polymorphism predisposes to immunologically mediated renal disease in 2 mammalian species provides direct evidence for the importance of genome plasticity in the evolution of genetically complex phenotypes, including susceptibility to common human disease. This assay has high sensitivity and excellent specificity for detection of Human FcGRIII. No significant cross-reactivity or interference between Human FcGRIII and analogues was observed.
Method Sandwich ELISA
Detection Range 0.312-20 ng/mL
Sensitivity 0.135 ng/mL
Reactivity Human
Sample Types Serum, Plasma, Other biological fluids.
Background Aitman et al. showed that copy number variation of the orthologous rat and human Fcgr3 genes is a determinant of susceptibility to immunologically mediated glomerulonephritis. Positional cloning identified loss of the rat-specific Fcgr3 paralog 'Fcgr3-related sequence' (Fcgr3rs) as a determinant of macrophage overactivity and glomerulonephritis in Wistar Kyoto rats. In humans, low copy number of FCGR3B, an ortholog of rat Fcgr3, was associated with glomerulonephritis in the autoimmune disorder systemic lupus erythematosus (SLE. Aitman et al. concluded that their finding that gene copy number polymorphism predisposes to immunologically mediated renal disease in 2 mammalian species provides direct evidence for the importance of genome plasticity in the evolution of genetically complex phenotypes, including susceptibility to common human disease.
Supplier Abebio

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