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Recombinant Mouse M-CSF R/CD115 Fc Chimera Protein, CF

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Product Details

Summary
Reactivity MuSpecies Glossary
Applications Bioactivity
Format
Carrier-Free

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Recombinant Mouse M-CSF R/CD115 Fc Chimera Protein, CF Summary

Details of Functionality
Measured by its ability to inhibit the M-CSF-induced proliferation of M‑NFS‑60 mouse myelogenous leukemia lymphoblast cells. Halenbeck, R. et al. (1989) Biotechnology 7:710. The ED50 for this effect is 0.2-0.8 µg/mL in the presence of 10 ng/mL mouse M-CSF.
Source
Mouse myeloma cell line, NS0-derived mouse M-CSF R/CD115 protein
Mouse M-CSF R
(Ala20-Ser511)
Accession #P09581
IEGRMDP Mouse IgG2A
(Glu98-Lys330)
N-terminus C-terminus
Accession #
N-terminal Sequence
Ala20
Structure / Form
Disulfide-linked homodimer
Protein/Peptide Type
Recombinant Proteins
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.

Applications/Dilutions

Dilutions
  • Bioactivity
Theoretical MW
82.3 kDa (monomer).
Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
115-135 kDa, reducing conditions
Publications
Read Publications using
3818-MR in the following applications:

Packaging, Storage & Formulations

Storage
  • 12 months from date of receipt, ≤ -20 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, ≤ -20 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS.
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Reconstitution Instructions
Reconstitute at 100 μg/mL in sterile PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Mouse M-CSF R/CD115 Fc Chimera Protein, CF

  • 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 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).

  1. deParseval, N. et al. (1993) Nucleic Acids Res. 21:750.
  2. Rothwell, V.M. and L.R. Rohrschneider (1987) Oncogene Res. 1:311.
  3. Chitu, V. and E.R. Stanley (2006) Curr. Opin. Immunol. 18:39.
  4. Ross, F.P. and S.L. Teitelbaum (2005) Immunol. Rev. 208:88.
  5. Rovida, E. et al. (2001) J. Immunol. 166:1583.
  6. Yeung, Y. et al. (1998) J. Biol. Chem. 273:17128.
  7. Dai, X. et al. (2002) Blood 99:111.
  8. Faccio, R. et al. (2003) J. Clin. Invest. 111:749.
  9. Li, M. et al. (2004) J. Neurochem. 91:623.
  10. Mitrasinovic, O.M. et al. (2005) J. Neurosci. 25:4442.

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