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Mouse CSF1R / MCSF Receptor / CD115 Protein (His & Fc Tag)

AI323359,CD115,CSF-1R,Csfmr,Fim-2,Fms,M-CSF-R,M-CSFR

Catalog Number P50059-M03H
Organism Species Mouse
Host Human Cells
Synonyms AI323359,CD115,CSF-1R,Csfmr,Fim-2,Fms,M-CSF-R,M-CSFR
Molecular Weight The recombinant mouse CSF1R/Fc is a disulfide-linked homodimer. The reduced monomer comprises 740 amino acids and has a predicted molecular mass of 83.3 kDa. The apparent molecular mass of the protein is approximately 110 kDa in SDS-PAGE under reducing conditions due to glycosylation.
predicted N Ala 20
SDS-PAGE
Purity > 95 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the mouse CSF1R (Met1-Ser511) was fused with the C-terminal polyhistidine-tagged Fc region of human IgG1 at the C-terminus.
Bio-activity 1. Immobilized mouse CSF1-His (P51112-M08H) at 10 μg/ml (100 μl/well) can bind mouse CSF1R-Fch, The EC50 of mouse CSF1R-Fch is 0.04-0.1 μg/ml.
2. Measured by its ability to inhibit mouse CSF-induced proliferation of M‑NFS‑60 mouse myelogenous leukemia lymphoblast cells. The ED50 for this effect is typically 0.01-0.04 μg/mL in the presence of 3 ng/ml Recombinant Human M-CSF.
Research Area Cancer |Oncoprotein & suppressor & biomarker |Oncoprotein |Growth Factor & Receptor |Receptor Tyrosine Kinase (RTK)
Formulation Lyophilized from sterile PBS, pH 7.4
1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background M-CSFR encoded by the proto-oncogene c-fms is the receptor for colony stimulating factor 1 (CSF1R), a cytokine involved in the proliferation, differentiation, and activation of macrophages. This cell surface glycoprotein is consisted by an extracellular ligand-binding domain, a single membrane-spanning segment, and an intracellular tyrosine kinase domain. Binding of CSF1 activates the receptor kinase, leading to "autophosphorylation" of receptor subunits and the concomitant phosphorylation of a series of cellular proteins on tyrosine residues. CSF1R is a tyrosine kinase receptor that is absolutely required for macrophage differentiation and thus occupies a central role in hematopoiesis. CSF1 and its receptor (CSF1R, product of c-fms proto-oncogene) were initially implicated as essential for normal monocyte development as well as for trophoblastic implantation. This apparent role for CSF1/CSF1R in normal mammary gland development is very intriguing because this receptor/ligand pair has also been found to be important in the biology of breast cancer in which abnormal expression of CSF1 and its receptor correlates with tumor cell invasiveness and adverse clinical prognosis. Tumor cell expression of CSF1R is under the control of several steroid hormones (glucocorticoids and progestins) and the binding of several bHLH transcription factors, while tumor cell expression of CSF-1 appears to be regulated by other hormones, some of which are involved in normal lactogenic differentiation. However, studies have demonstrated that CSF1 and CSF1R have additional roles in mammary gland development during pregnancy and lactation. The role of CSF1 and CSF1R in normal and neoplastic mammary development that may elucidate potential relationships of growth factor-induced biological changes in the breast during pregnancy and tumor progression.
Reference
  • Sherr CJ. (1990) The colony-stimulating factor 1 receptor: pleiotropy of signal-response coupling. Lymphokine Res. 9(4): 543-8.
  • Kacinski BM. (1997) CSF-1 and its receptor in breast carcinomas and neoplasms of the female reproductive tract. Mol Reprod Dev. 46(1): 71-4.
  • Sapi E, et al. (1999) The role of CSF-1 in normal and neoplastic breast physiology. Proc Soc Exp Biol Med. 220(1): 1-8.
  • Sapi E. (2004) The role of CSF-1 in normal physiology of mammary gland and breast cancer: an update. Exp Biol Med (Maywood). 229(1): 1-11.
  • Bonifer C, et al. (2008) The transcriptional regulation of the Colony-Stimulating Factor 1 Receptor (csf1r) gene during hematopoiesis. Front Biosci. 13: 549-60.