Product Pathways - Tyrosine Kinase / Adaptors
M-CSF Receptor (E7S2S) Rabbit mAb #14582
|14582S||100 µl ( 10 western blots )||￥3,100.00 现货查询||购买询价|
|14582||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting,
Specificity / Sensitivity
M-CSF Receptor (E7S2S) Rabbit mAb recognizes endogenous levels of total M-CSF receptor protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly92 of human M-CSF receptor protein.
Macrophage-colony stimulating factor (M-CSF, CSF-1) receptor is an integral membrane tyrosine kinase encoded by the c-fms proto-oncogene. M-CSF receptor is expressed in monocytes (macrophages and their progenitors) and drives growth and development of this blood cell lineage. (1-3). Binding of M-CSF to its receptor induces receptor dimerization, activation, and autophosphorylation of cytoplasmic tyrosine residues used as docking sites for SH2-containing signaling proteins (4). There are at least five major tyrosine autophosphorylation sites. Tyr723 (Tyr721 in mouse) is located in the kinase insert (KI) region. Phosphorylated Tyr723 binds the p85 subunit of PI3 kinase as well as PLCγ2 (5). Phosphorylation of Tyr809 provides a docking site for Shc (5). Overactivation of this receptor can lead to a malignant phenotype in various cell systems (6). The activated M-CSF receptor has been shown to be a predictor of poor outcome in advanced epithelial ovarian carcinoma (7) and breast cancer (8).
After initial dimerization and autophosphorylation, the M-CSF receptor undergoes a regulated intramembrane proteolysis (RIP) involving two cleavage events. Extracellular cleavage of this membrane protein results in release of the extracellular domain, while cleavage in the transmembrane region releases the cytoplasmic domain into the cytosol (9). The activated intracellular domain localizes to the nucleus to regulate transcription of specific pro-inflammatory genes (10). Research studies indicate that the processing and down regulation of M-CSF receptor is a continuous process whose rate increases in response to various stimuli, including PMA, LPS, tumor necrosis factor, IL-2, Il-4, and the physiological ligand M-CSF (9).
- Stanley, E.R. et al. (1978) Nature 274, 168-70.
- Byrne, P.V. et al. (1981) J Cell Biol 91, 848-53.
- Bourette, R.P. and Rohrschneider, L.R. (2000) Growth Factors 17, 155-66.
- Novak, U. et al. (1996) Oncogene 13, 2607-13.
- Bourette, R.P. et al. (1997) EMBO J 16, 5880-93.
- Morley, G.M. et al. (1999) Oncogene 18, 3076-84.
- Toy, E.P. et al. (2001) Gynecol Oncol 80, 194-200.
- Maher, M.G. et al. (1998) Clin Cancer Res 4, 1851-6.
- Wilhelmsen, K. and van der Geer, P. (2004) Mol Cell Biol 24, 454-64.
- Glenn, G. and van der Geer, P. (2007) FEBS Lett 581, 5377-81.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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