NF-κB Reporter (Luc) - CHO-K1 Recombinant Cell Line
An NF-κB luciferase reporter construct is stably integrated into the genome of CHO-K1 cells. The firefly luciferase gene is controlled by the NF-κB response element located upstream of the TATA promoter. Following activation by stimulants, endogenous NF-κB transcription factors bind to the DNA response elements to induce transcription of the luciferase gene.
The NF-κB-luciferase / CHO-K1 cell line is suitable for monitoring the activity of NF-κB transcription factor through luminescence readout.). This cell line responds to human cytokine IL-1β, responds moderately to human TNF, and does not respond to human IFN-λ (2 μg/ml). Reducing the amount of serum during incubation period may increase the sensitivity to cytokines. Since CHO-K1 cells do not express endogenous human proteins, this cell line provides an excellent platform to enable exogenous expression of a protein of interest to study its downstream effect on NF-κB signaling.
Interested in screening and profiling inhibitors, blocking antibodies, or activators of NF-κB-mediated signaling without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening.
This product has been cited 1 time.
Purchase of this cell line is for research purposes only; commercial use requires a separate license. View the full terms and conditions.
1. Delude, R.L., et.al. (1994) CD14-mediated Translocation of Nuclear Factor-kB Induced by Lipopolysaccharide Does Not Require Tyrosine Kinase Activity. J. Biol. Chem. 269: 22253
2. Railo, A., et.al. (2008) Wnt-11 signaling leads to down-regulation of the Wnt/betacatenin, JNK/AP-1 and NF-kappaB pathways and promotes viability in the CHO-K1 cells. Exp Cell Res. 314: 2389-99
3. Murphy, S.H., et.al. (2011) Tumor suppressor protein (p)53, is a regulator of NF-κB repression by the glucocorticoid receptor. Proc. Natl. Acad. Sci. USA 108: 17117-17122
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