Notch1/CSL Luciferase Reporter HEK293 Cell Line
The Notch1/CSL Luciferase Reporter HEK293 Cell Line is a HEK293 cell line that expresses the firefly luciferase reporter under the control of Notch-response elements (CSL responsive elements) and expression of Notch1DE (Notch1 that has a deletion of the entire extracellular domain). Inside the cells, the Notch1DE can be cleaved by γ-secretase. This active Notch1 NICD (Notch intracellular domain) translocated to the nucleus and induces the expression of the luciferase reporter. The cell line is validated for the inhibition of the expression of luciferase reporter using a known inhibitor of the Notch signaling pathway.
Interested in screening and profiling inhibitors, blocking antibodies, or activators of the Notch1 pathway without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening.
This product has been cited 5 times.
Purchase of this cell line is for research purposes only; commercial use requires a separate license. View the full terms and conditions.
Media Required for Cell Culture
| Name | Ordering Information |
| Thaw Medium 1 | BPS Bioscience #60187 |
| Growth Medium 1A | BPS Bioscience #79528 |
Materials Required for Cellular Assays
| Name | Ordering Information |
| DAPT | Selleckchem #S2215 |
| CSL Reporter HEK293 Cell Line | BPS Bioscience #79754 |
| Thaw Medium 1 | BPS Bioscience #60187 |
| 96-well tissue culture-treated white clear-bottom assay plate | |
| One-Step™ Luciferase Assay System | BPS Bioscience #60690 |
| Luminometer |
The cell line has been screened to confirm the absence of Mycoplasma species.
The Notch signaling pathway controls cell fate decisions in vertebrates and invertebrates’ tissues and is involved in embryonic development, tissue homeostasis, and regulation of the immune and angiogenic systems. Notch signaling is triggered through the binding of a transmembrane ligand, present in opposing cells, to one of the four existing Notch transmembrane receptors (Notch1/Notch2/Notch3/Notch4). This results in proteolytic cleavage of the Notch receptor, releasing the constitutively active intracellular domain of the Notch receptor (NICD). NICD translocate to the nucleus and associates with the transcription factor CSL (CBF1/RBPJκ/Suppressor of Hairless/Lag-1) and coactivator Mastermind to turn on the transcription of Notch-responsive genes. Dysfunction of Notch signaling has severe consequences, including developmental pathologies or cancer (such as T cell acute lymphoblastic leukemia, T-ALL, and urothelial bladder cancer). The use of Notch inhibitors, mainly gammasecretase inhibitors, as a cancer therapy option and in the regeneration of tissues is ongoing. Further studies will allow us to have a deeper understanding of Notch signaling and will benefit future therapeutic approaches.
1. Lu, FM et al. (1996). Proc. Natl. Acad. Sci. USA 93(11): 5663-5667.
2. Kanungo, et al. (2008). J. Neurochem. 106: 2236.
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