The CSF1R SRE HEK293 recombinant cell line has been transfected with full-length human CSF1R cDNA (NP_005202) under a CMV promoter for high constitutive expression. The SRE-luciferase reporter is also stably integrated into the genome. The firefly luciferase gene is controlled by 4 copies of the Serum Response Element upstream of a minimal promoter. Upon ligand binding, active CSF1R will initiate the MAPK/ERK signaling pathway, leading to expression of the SRE-controlled luciferase reporter.
Host Species: human
Supplied as Two vials containing ~ 2 x 106 cells in 1 ml of 10% DMSO in FBS.
Background
Colony Stimulating Factor 1 Receptor (CSF1R, CSFR, CD115, M-CSF-R) is a single-pass tyrosine kinase transmembrane receptor which is part of the type III protein tyrosine kinase receptor family. CSF1R is activated by either of two cytokines, CSF1 (MCSF; CSF-1) and IL-34 (IL34), causing homodimerization and activation of downstream kinase activity. CSF1R is expressed on the surface of monocytes and macrophages, and its activation controls the growth, function, and differentiation of macrophages. This interaction is used by numerous cancer types, such as diffuse-type tenosynovial giant cell tumors (dt-GCT), to evade the immune system. By overexpressing the cytokine CSF1, these cells drive the development and survival of Tumor-Associated Macrophages (TAMs), which in turn suppress the local immune response to the cancer.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.
Application
Monitor the CSF1R/MAPK/ERK signaling pathway activity and SRF-mediated activity. Screen for activators or inhibitors of the CSF1R/MAPK/ERK signaling pathway.
Host Cell
HEK293
Synonyms
CSF1R, CSFR, CD115, M-CSF-R
Shipping Temperature
-80°C (dry ice)
Note
License Disclosure: Purchase of this cell line grants you with a 10-year license to use this cell line in your immediate laboratory, for research use only. This license does not permit you to share, distribute, sell, sublicense, or otherwise make the cell line available for use to other laboratories, departments, research institutions, hospitals, universities, or biotech companies. The license does not permit use of this cell line in humans or for therapeutic or drug use. The license does not permit modification of the cell line in any way. Inappropriate use or distribution of this cell line will result in revocation of the license and result in an immediate cease of sales and distribution of Biohippo products to your laboratory. Biohippo does not warrant the suitability of the cell line for any particular use, and does not accept any liability in connection with the handling or use of the cell line. Modifications of this cell line, transfer to another facility, or commercial use of the cells may require a separate license and additional fees; contact [email protected] for details. Publications using this cell line should reference Biohippo Inc. Warning: Avoid multiple freeze/thaw cycles.
Storage Stability
Store in liquid nitrogen immediately upon receipt. Do not store for long-term at -80°C or on dry ice.
Reference
1. Cannarile, Michael A., et al. 2017. “Colony-Stimulating Factor 1 Receptor (CSF1R) Inhibitors in Cancer Therapy.” Journal for Immunotherapy of Cancer, 5(1),(53), doi:10.1186/s40425-017-0257-y. 2. Liu, Yang, and Xuetao Cao. 2014. “The Origin and Function of Tumor-Associated Macrophages.” Cellular and Molecular Immunology, 12(1), 1-4., doi:10.1038/cmi.2014.83. 3. Luo, Jian, et al. 2013. “Colony-Stimulating Factor 1 Receptor (CSF1R) Signaling in Injured Neurons Facilitates Protection and Survival.” The Journal of Experimental Medicine, 210(1), 157-172., doi:10.1084/jem.20120412. 4. Yao, G.-Q., et al. 2005. “CSF-1 Induces Fos Gene Transcription and Activates the Transcription Factor Elk-1 in Mature Osteoclasts.” Calcified Tissue International, 76(5), 371-378., doi:10.1007/s00223-004-0099-8.