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FLuc Reporter Cell Line - HCT116

FLuc Reporter Cell Line - HCT116

Cat.No. :  CSC-RR0266-F Host Cell:  HCT116

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Cat. No. CSC-RR0266-F
Description This cell line is engineered to stably overexpress Firefly Luciferase (FLuc) reporter gene. It is an ideal positive control for use in bioluminescence assays. In addition, HCT116 cells can form tumors in mouse. The in vivo growth of these tumors can be monitored using bioluminescent imaging.
Gene Fluc
Host Cell HCT116
Host Cell Species Homo sapiens (Human)
Stability Validated for at least 10 passages
Application

1. Gene expression studies

2. Protein localization

3. Drug screening and toxicology

4. Live cell imaging

Quality Control Negative for bacteria, yeast, fungi and mycoplasma.
Shipping Dry ice
Storage Liquid nitrogen
Revival Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media.
Mycoplasma Negative
Format One frozen vial containing millions of cells
Storage Liquid nitrogen
Safety Considerations

The following safety precautions should be observed.

1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum.

2. No eating, drinking or smoking while handling the stable line.

3. Wash hands after handling the stable line and before leaving the lab.

4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells.

5. All waste should be considered hazardous.

6. Dispose of all liquid waste after each experiment and treat with bleach.

Ship Dry ice
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While the MDM2-p53 interaction has been extensively documented, MDM2 overexpression is observed in human cancers with little or no functional p53, indicating that mdm2 expression is regulated by mechanisms independent of p53. Researchers reveal NFAT1's novel role in cancer biology by demonstrating its direct regulation of MDM2 expression. NFAT1 binds to the mdm2 P2 promoter, increasing mdm2 transcription independently of p53. This leads to elevated MDM2 levels, impairing p53 function in DNA damage response. The study highlights NFAT signaling dysregulation in cancer and its association with MDM2 overexpression in hepatocellular carcinoma tissues. It suggests NFAT1 as a potential therapeutic target and prompts further research into cancer development and therapy.

The role of NFAT1 in mdm2 transcription regulation was investigated using Luc Reporter Cell Line-HCT116. HCT116 (p53 and p53) cells were transfected with the NFAT1 plasmid, and mdm2 mRNA levels were measured. Additionally, mdm2 promoter activity was assessed by co-transfecting the NFAT1 plasmid with a luciferase reporter vector, and luciferase levels were quantified. Results suggest NFAT1 involvement in mdm2 transcriptional regulation, providing insights into cellular processes.Figure 1. The role of NFAT1 in mdm2 transcription regulation was investigated using Luc Reporter Cell Line-HCT116. HCT116 (p53+/+ and p53−/−) cells were transfected with the NFAT1 plasmid, and mdm2 mRNA levels were measured. Additionally, mdm2 promoter activity was assessed by co-transfecting the NFAT1 plasmid with a luciferase reporter vector, and luciferase levels were quantified. Results suggest NFAT1's involvement in mdm2 transcriptional regulation, providing insights into cellular processes. (Zhang X, et al., 2012)

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