THP-1/STAT3 Reporter (Luc) Stable Cell Line

Description

THP-1/STAT3 Reporter (Luc) Stable Cell Line is a genetically engineered human monocytic cell line designed to monitor STAT3 (Signal Transducer and Activator of Transcription 3) signaling activity through luciferase (Luc) reporter expression. Derived from THP-1 cells, the cell line maintains key native THP-1 characteristics, such as the capacity to upregulate CD14 upon differentiation and PMA-induced differentiation into macrophage-like cells, while featuring a luciferase reporter system under the control of STAT3-responsive elements. The cell line enables sensitive quantification of STAT3 pathway activation through bioluminescence measurement, making it particularly valuable for studying inflammatory responses, immune regulation, and oncogenic signaling research. Cells exhibit dose-dependent luciferase activity upon STAT3 activation while retaining their original biological properties, allowing for high-throughput screening applications and kinetic studies of STAT3 signaling dynamics. Maintained at low passage numbers (<P20) to ensure reporter stability and consistent performance, this cell line provides a reliable tool for immunology and cancer research. The cells are rigorously tested to ensure they are free of contamination from HIV-1, HBV, HCV, Syphilis, mycoplasma, Fungi, Yeast and Bacteria.

Application

• FOR RESEARCH USE ONLY
  

• The THP-1/STAT3 Reporter (Luc) Stable Cell Line is a human monocytic cell model engineered to monitor STAT3 signaling activity through luciferase reporter expression. This system enables sensitive, quantitative detection of STAT3 pathway activation in response to cytokines (e.g., IL-6, IL-10) or JAK-STAT inhibitors via bioluminescence imaging. The cell line retains native THP-1 characteristics while providing dynamic readouts for inflammation research, cancer immunology studies, and drug screening applications. Maintain in RPMI-1640 with 10% FBS and selection antibiotics to ensure stable reporter performance during investigations of immune signaling pathways.