- Species ReactivityMouse
- SpecificityDetects mouse M-CSF R/CD115 in direct ELISAs and Western blots. In direct ELISAs, approximately 40% cross-reactivity with recombinant human M-CSF R/CD115 is observed.
- SourcePolyclonal Sheep IgG
- PurificationAntigen Affinity-purified
- ImmunogenMouse myeloma cell line NS0-derived recombinant mouse M-CSF R/CD115
Ala20-Ser511
Accession # P09581 - FormulationLyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied as a 0.2 µm filtered solution in PBS.
- LabelUnconjugated
- Western Blot0.1 µg/mLRecombinant Mouse M-CSF R/CD115 Fc Chimera (Catalog # 3818-MR)
- Immunocytochemistry5-15 µg/mLSee below
- ReconstitutionReconstitute at 0.2 mg/mL in sterile PBS.
- ShippingThe product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
- Stability & StorageUse a manual defrost freezer and avoid repeated freeze-thaw cycles.
- 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.
- 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.
- Long Name:Macrophage Colony Stimulating Factor Receptor
- Entrez Gene IDs:1436 (Human)
- Alternate Names:CD115 antigen; CD115; c-fms; colony stimulating factor 1 receptor; CSF1R; CSF-1-R; CSFR; EC 2.7.10.1; FMS proto-oncogene; FMSFIM2; macrophage colony stimulating factor I receptor; macrophage colony-stimulating factor 1 receptor; McDonough feline sarcoma viral (v-fms) oncogene homolog; M-CSF R; MCSFR; M-CSFR; Proto-oncogene c-Fms
Background:
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). Mouse M-CSF receptor cDNA encodes 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 mouse M-CSF R ECD shares > 99% aa identity with rat and 60-63% aa identity with corresponding sequences in human, canine, feline and bovine M-CSF R. 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 integrinalpha 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 betapeptide, but their role in pathogenesis is unclear (9, 10).
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