MAPK/JNK/AP-1
Principle
The AP-1 (Activator Protein-1) transcription factor complex is a master regulator of cellular fate, governing proliferation, differentiation, transformation, and apoptosis. Primarily composed of c-Jun and Fos heterodimers, AP-1 selectively binds to TPA-responsive elements (TREs) within DNA to drive downstream gene expression.
Because AP-1 integrates signals from several major upstream pathways including JNK, ERK, and MAPK, it serves as a definitive readout for intracellular signaling events. This cell line allows researchers to monitor activation triggered by a diverse range of stimuli:
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Cytokines: TNF-alpha, IL-1
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Growth Factors & Serum: EGF, FGF, and FBS induction
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Environmental Stress: UV radiation, oxidative stress, and osmotic shock
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Oncogenic Factors: TPA/PMA and viral protein expression
To support pathway analysis, Signosis has developed a stable AP‑1 luciferase reporter cell lines. Clonal selection ensures strong and reproducible luciferase induction in response to stimuli such as PMA. This validated reporter system provides a reliable, ready‑to‑use platform for examining AP‑1 activation triggered by cytokines, gene perturbation, or other experimental treatment. The cell line can be used as a reporter system for monitoring the activity of AP-1 triggered by stimuli treatment, such as TNFa, IL-1, gene overexpression and gene knockdown. The cells contain no viral particles.
Key Benefits
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High Sensitivity & Responsiveness: Each cell line is validated to induce a strong reporter signal in response to stimuli.
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Consistent: TF reporter construct is stably integrated into the genome to avoid experimental/cell-to-cell variations.
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Proven Stability: Signosis has engineered these stable reporter cell lines through rigorous clonal selection, ensuring consistent and reproducible luciferase induction across multiple passages.
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Time-Saving: Cell line can be used for experiments right away to study different signaling pathways.
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Routine Quality Testing: All cell lines test negative for mycoplasma or viral particles.
