Mouse Meteorin-Like Protein ELISA Kit from MyBioSource.com

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Mouse Meteorin-Like Protein ELISA Kit

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Description

This Mouse Meteorin-Like Protein ELISA Kit is intended for quantitative detection of mouse Meteorin-like in cell culture supernates, cell lysates, serum and plasma (heparin, EDTA). Strip well format. Reagents for up to 96 tests.
This mouse Meteorin-like ELISA Kit was based on standard sandwich enzyme-linked immune-sorbent assay technology. A monoclonal antibody from rat specific for Meteorin-like has been precoated onto 96-well plates. Standards (Expression system for standard: NSO, Immunogen sequence: Q46-E311) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for Meteorin-like is added subsequently and then followed by washing with PBS or TBS buffer. Avidin-Biotin-Peroxidase Complex was added and unbound conjugates were washed away with PBS or TBS buffer. HRP substrate TMB was used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the mouse Meteorin-like amount of sample captured in plate.
The capture antibody is a monoclonal antibody from rat, the detection antibody is a biotinylated polyclonal antibody from goat. Expression system for standard: METRNL (Meteorin-like) is a cytoplasmic 30 kDa (predicted) member of the meteorin family of proteins. It is expressed by neurons, and appears to function as a primer molecule that sets the stage for either cell differentiation or neurite outgrowth when it acts with Dclk1 and SerpinB1. In mice, exogenously elevated circulating Metrnl increased whole-body energy expenditure and improved glucose tolerance following diet-induced obesity. It also induced expression of antiinflammatory genes, leading to alternative activation of macrophages in adipose tissue and to browning of white fat depots. Metrnl did not appear to activate thermogenic genes directly, but it stimulated eosinophils and macrophages to enter adipose tissue and take their specific thermogenic actions. Blockade of cytokine signaling eliminated Metrnl-induced changes in gene expression required for alternative macrophage activation and blunted expression of beige fat thermogenic and beta-oxidation genes. It is concluded that METRNL is a hormone that influences energy expenditure and thermogenic programs in adipose tissue