FM-E100331
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Mouse CSF1R/M-CSFR ELISA Kit
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Assay Range | 62.5--4000 pg/mL |
Sensitivity | 10.0 pg/mL |
Size | 96T |
Storage | Store at 2 - 8ºC. Keep reconstituted standard and detection Ab at -20 ºC |
Assay Principle | Sandwich ELISA |
Sample volume | 100 µL final volume, dilution factor varies on samples |
Detection Method | Chromogenic |
Kit Components
1. Recombinant Mouse CSF1R standard: 2 vials
2. One 96-well plate precoated with anti- Mouse CSF1R Ab
3. Sample diluent buffer: 12 mL - 1
4. Detection antibody: 130 µL, dilution 1:100
5. Streptavidin-HRP: 130 µL, dilution 1:100
6. Antibody diluent buffer: 12 mL x1
7. Streptavidin-HRP diluent buffer: 12 mL x1
8. TMB developing agent: 10 mL x1
9. Stop solution: 10 mL x1.
10. Washing solution (20x): 25 mL x1.
Background
M-CSF receptor (macrophage colony-stimulating factor 1 receptor, M-CSFR, CSF-1-R), also known as proto-oncogene c-Fms, or CD115, is a member of the type III subfamily of receptor tyrosine kinases. This protein group, including receptors for PDGF and SCF, is characteristic of five immunoglobulin-like domains in their extracellular domain (ECD) and a split kinase domain in their intracellular region. Mouse MCSF receptor is synthesized as a 977 amino acid (aa) type I membrane protein with a 19 aa signal peptide, a 492 aa extracellular region containing the ligand binding domain, a 25 aa transmembrane domain and a 441 aa cytoplasmic domain. The ECD of mouse MCSF R shares more than 99% and 60% aa identity with rat and human counterparts, respectively. M-CSF binding initiates M-CSFR homodimerization, phosphorylation and activation of a series of signaling molecules, especially PI3 Kinase, P42/44 ERK and cCbl, that play an important role in cell proliferation, survival, differentiation and cytoskeletal reorganization. M-CSF/M-CSFR signaling is continuously required for macrophage survival and regulates lineage decisions and maturation of monocytes, macrophages, osteoclasts and DC. It is reported that M-CSFR and integrin αvβ3 share signaling pathways during osteoclastogenesis and deletion of either causes osteopetrosis.