CSF1R/SRE-Luc/HEK293
CBP74010
| I. Background | |
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Colony Stimulating Factor 1 Receptor (CSF1R, CD115, M-CSF-R) is the receptor for the cytokine CSF1 (MCSF; CSF-1), which controls the growth, function, and differentiation of macrophages. This interaction drives the development and survival of Tumor-Associated Macrophages (TAMs), which in turn suppress the local immune response to the cancer. An alternative ligand is IL-34, which has been implicated in neuroprotective and survival signals following brain injury and neurodegeneration. As a tyrosine kinase transmembrane receptor, activation of CSF1R by its ligand initiates a vast array of intracellular activity, including activation of the MAPK/ERK signaling pathway. When phosphorylated by ERK, Elk1 forms a complex with Serum Response Factor (SRF) and binds to Serum Response Element (SRE), resulting in the expression of numerous mitogen-inducible genes. |
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| Ⅱ. Introduction | |
| Host Cell: | HEK293 |
| Expressed gene: | CFS1R-SRE-Luciferase |
| Stability: | 32 passages (in-house test, that not means the cell line will be instable beyond the passages we tested.) |
| Synonym(s): | FMS, CD115 |
| Freeze Medium: | 90% FBS+10% DMSO |
| Culture Medium: | DMEM +10%FBS+200ug/ml hygromycin+1ug/ml puromycin |
| Mycoplasma Testing: | Negative |
| Storage: | Liquid nitrogen |
| Application(s): | Functional(Report Gene) Assay |
| Ⅲ. Description of Host Cell Line | |
| Organism: | Human |
| Tissue: | Embryonic kidney |
| Morphology: | Epitheloid cell |
| Growth Properties: | Adherent |
| Ⅳ. Representative Data | |
Figure 1. Recombinant HEK293 cell line expressing firefly luciferase gene under the control of SRE response elements with constitutive expression of CSF1R(Colony Stimulating Factor 1 Receptor)
Figure 2. Detect Luciferase assay by Ultra Luciferase Detection Kit CBPH0001（we strongly suggest to purchase from Cobioer). HEK293/CFS1R-SRE Luciferase Reporter cells were stimulated by CSF1, the EC50 was 3.75ng/ml.
Figure 3. Inhibition of CSF1 (100 ng/ml) -induced SRE reporter actity by CSF1R inhibitors.
