Rat MCSF (Macrophage Colony Stimulating Factor 1) ELISA Kit (E-EL-R3083)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Rat MCSF. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Rat MCSF and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Rat MCSF, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Rat MCSF. You can calculate the concentration of MCSF in the samples by comparing the OD of the samples to the standard curve.

M-CSF, also known as CSF-1, is a four-α-helical-bundle cytokine that is the primary regulator of macrophage survival, proliferation, and differentiation. M-CSF is found as isoforms of various sizes. All isoforms contain the N-terminal 150 amino acid (aa) portion that is necessary and sufficient for interaction with the M-CSF receptor but may vary in activity and half-life.Sources of M-CSF include fibroblasts, activated macrophages, endometrial secretory epithelium, bone marrow stromal cells, vitamin D-stimulated osteoblasts, and activated endothelial cells. The M-CSF receptor (M-CSF R, also called c-fms) transduces the pleotropic effects of M-CSF and mediates its endocytosis. Engagement of M-CSF dimers by M-CSF R induces receptor dimerization, followed by phosphorylation at multiple sites. M-CSF R is expressed on monocytes and tissue macrophages, and treatment with M-CSF promotes differentiation of macrophages, kidney mesangial cells, liver Kupffer cells, brain microglial cells, bone osteoclasts, fetal trophoblast cells, skin Langerhans cells, intestinal Paneth cells, and blood and lymph node plasmacytoid dendritic cells. M-CSF R is also expressed on osteoblasts where it downregulates RANKL production, thus allowing M-CSF to limit osteoclast production. M-CSF is essential for macrophage-related functions such as bone resorption, vascular development, and innate immunity. M-CSF regulates the release of cytokines and other inflammatory modulators from macrophages, and stimulates chemotaxis and pinocytosis. Circulating M-CSF increases during pregnancy and supports implantation and growth of the decidua and placenta. M-CSF expression can also be increased during infection or in inflammatory disorders such as inflammatory bowel disease. Both M-CSF and its receptor can be expressed by a number of cancers, allowing M-CSF to act as an autocrine growth factor for cancer cells. Macrophages can also be recruited to tumor tissues, supplying M-CSF as a paracrine growth factor. On the other hand, M-CSF can have anti-cancer effects by priming and enhancing macrophage killing of tumor cells and microorganisms.