THP-1 SMAD/TGF β Reporter (Luc) Stable Cell Line

Description

THP-1 SMAD/TGF β Reporter (Luc) Stable Cell Line is a genetically engineered human monocytic cell line designed to monitor SMAD-dependent TGF β (Transforming Growth Factor Beta) signaling 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 SMAD-responsive elements. The cell line enables sensitive quantification of TGF β pathway activation through bioluminescence measurement, making it particularly valuable for studying immune regulation, fibrosis mechanisms, and cancer microenvironment research. Cells exhibit dose-dependent luciferase activity upon TGF β stimulation while retaining their original biological properties, allowing for high-throughput drug screening and mechanistic studies of SMAD 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 translational medicine 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 SMAD/TGF β Reporter (Luc) Stable Cell Line is a human monocytic cell model engineered to monitor TGF β/SMAD signaling pathway activity through luciferase reporter expression. This system enables quantitative detection of TGF β-mediated SMAD activation in response to ligands (e.g., TGF β1-3), inflammatory stimuli, or pathway inhibitors via bioluminescence imaging. The cell line retains THP-1 differentiation capacity while providing dynamic readouts for studying immunoregulation, fibrosis mechanisms, and cancer-associated macrophage polarization. Maintain in RPMI-1640 with 10% FBS and selection antibiotics to ensure stable reporter function during investigations of TGF β signaling in immunological processes.