STAT3 Reporter Jurkat Cell Line
The STAT3 Reporter Jurkat cell line is designed for monitoring the STAT3 signal transduction pathway. It contains a firefly luciferase gene driven by STAT3 response elements located upstream of the minimal TATA promoter. After activation by cytokines or growth factors that act on the receptor, endogenous STAT3 translocate to the nucleus and binds to the DNA response elements, inducing transcription of the luciferase reporter.
This cell line responds to human interferons IFN-α and IFN-γ but not to interleukins IL-6, IL-1α, IL-2, or TNF-α. Activation of the STAT3 pathway by IFN-α is inhibited by JAK inhibitor CP 690,550.
Figure 1: Mechanism of STAT3 Reporter Jurkat Cell Line response to activation.
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 2 | BPS Bioscience #60184 |
| Growth Medium 2K | BPS Bioscience #78078 |
Materials Required for Cellular Assay
| Name | Ordering Information |
| Thaw Medium 2 | BPS Bioscience #60184 |
| Human IFN-alpha A | R&D Systems #11100-1 |
| Human IFN-γ | R&D Systems #285-IF |
| IL-6 | R&D Systems #206-IL |
| IL-1α | R&D Systems #200-LA |
| IL-2 | StemCell #78036 |
| TNF-α | R&D Systems #210-TA |
| Pan-JAK inhibitor CP 690,550 | Cayman #11598 |
| ONE-Step™ Luciferase Assay System | BPS Bioscience #60690 |
| Luminometer |
The cell line has been screened to confirm the absence of Mycoplasma species.
The JAK-STAT (Janus kinase signal transducer and activator of transcription) signaling pathway is involved in hematopoiesis, differentiation, metabolism, and immune response, and is responsive to more than 50 cytokines and growth factors. Once a ligand is bound to the receptor, JAKs will recruit STATs. Phosphorylated STATs will dimerize and translocate to the nucleus where they regulate gene transcription. Abnormal JAK-STAT function leads to diseases ranging from rheumatoid arthritis (RA), atopic dermatitis (AD), hematological disorders and other cancer types. This pathway has been an attractive target for drug discovery, with several JAK inhibitors currently approved for clinical use (example, ruxolitinib). In the context of immune regulation, STAT3 is expressed in diverse cell types. While it was initially described as an acute phase response factor in the context of IL-6 signaling, STAT3 has since been identified as a downstream regulator of many cytokines. STAT3 can also be activated downstream of Type1 Interferons, such as IFN-alpha, where it may function as a negative regulator of Type1 interferon signaling. Further studies of the JAK-STAT signaling pathways can prove useful in deepening our understanding of immunological diseases and cancer.
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