Farnesoid X receptor (FXR, NR1H4) is a member of the nuclear hormone receptor superfamily. These nuclear hormone receptors are ligand-activated transcription factors that elicit their actions by binding to hormone response elements (HREs) in the promoters of target genes and regulating transcription in response to lipophilic ligands.
 
Similar to other nuclear receptors, when activated, FXR translocates to the cell nucleus, forms a dimer with RXR and binds to hormone response elements on DNA, which up- or down-regulates the expression of certain genes, involved in lipid and glucose homeostasis which play a crucial role in pathophysiology of many major diseases such as diabetes, obesity, atherosclerosis and heart failure. In addition, FXR activation has been shown to be critical in the regulation of inflammatory responses.
 
Signosis now offers FXR-Luciferase reporter stable cell line to the research community. This high-quality stable cell lines will facilitate further molecular studies of FXR pathway and its functions.
 
Principle behind TF luciferase reporter. TF luciferase reporter stable cell line utilizes artificial promoter constructs to drive luciferase expression. The promoter region can consists of multiple repeats of a cis-element TF binding site, a DNA fragment from the promoter region of a known TF downstream gene, or a DNA fragment containing putative/known TF binding sites. There are several ways that a TF can be activated, such as through extracellular stimuli or through intracellular signaling pathways. Once activated, the TF translocates to the nucleus and often interacts with relevant co-factors to drive gene expression. Once luciferase is expressed, it can generate light in an enzymatic assay and the amount of light measured is positively correlated with the level of TF activation.