Human M-CSF R/CD115 Antibody Summary
Ile20-Glu512 (Pro54Ala)
Accession # P07333.2
Applications
Human M-CSF R/CD115 Sandwich Immunoassay
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: M-CSF R/CD115
M-CSF receptor, the product of the c-fms proto-oncogene, is a member of the type III subfamily of receptor tyrosine kinases that also includes receptors for SCF and PDGF. These receptors each contain five immunoglobulin-like domains in their extracellular domain (ECD) and a split kinase domain in their intracellular region (1-4). M-CSF receptor is expressed primarily on cells of the monocyte/macrophage lineage, dendritic cells, stem cells and in the developing placenta (1). Human M-CSF receptor cDNA encodes a 972 amino acid (aa) type I membrane protein with a 19 aa signal peptide, a 493 aa extracellular region containing the ligand-binding domain, a 25 aa transmembrane domain and a 435 aa cytoplasmic domain. The human M-CSF R ECD shares 60%, 64%, 72%, 75%, 75%, and 76% aa identity with mouse, rat, bovine, canine, feline and equine M-CSF R, respectively. Activators of protein kinase C induce TACE/ADAM17 cleavage of the M-CSF receptor, releasing the functional ligand-binding extracellular domain (5). M-CSF binding induces receptor homodimerization, resulting in transphosphorylation of specific cytoplasmic tyrosine residues and signal transduction (6). The intracellular domain of activated M-CSF R binds more than 150 proteins that affect cell proliferation, survival, differentiation and cytoskeletal reorganization. Among these, PI3Kinase, P42/44 ERK and c-Cbl are key transducers of M-CSF R signals (3, 4). M-CSF R engagement is continuously required for macrophage survival and regulates lineage decisions and maturation of monocytes, macrophages, osteoclasts and DC (3, 4). M-CSF R and integrin alpha v beta 3 share signaling pathways during osteoclastogenesis and deletion of either causes osteopetrosis (7, 8). In the brain, microglia expressing increased M-CSF R are concentrated with Alzheimers a beta peptide, but their role in pathogenesis is unclear (9, 10).
- deParseval, N. et al. (1993) Nucleic Acids Res. 21:750.
- Rothwell, V.M. and L.R. Rohrschneider (1987) Oncogene Res. 1:311.
- Chitu, V. and E.R. Stanley (2006) Curr. Opin. Immunol. 18:39.
- Ross, F.P. and S.L. Teitelbaum (2005) Immunol. Rev. 208:88.
- Rovida, E. et al. (2001) J. Immunol. 166:1583.
- Yeung, Y. et al. (1998) J. Biol. Chem. 273:17128.
- Dai, X. et al. (2002) Blood 99:111.
- Faccio, R. et al. (2003) J. Clin. Invest. 111:749.
- Li, M. et al. (2004) J. Neurochem. 91:623.
- Mitrasinovic, O.M. et al. (2005) J. Neurosci. 25:4442.
Product Datasheets
Citation for Human M-CSF R/CD115 Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
1 Citation: Showing 1 - 1
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Vimseltinib: A Precision CSF1R Therapy for Tenosynovial Giant Cell Tumors and Diseases Promoted by Macrophages
Authors: Bryan D. Smith, Michael D. Kaufman, Scott C. Wise, Yu Mi Ahn, Timothy M. Caldwell, Cynthia B. Leary et al.
Molecular Cancer Therapeutics
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