Principle 

SMAD proteins are transcription factors that respond to transforming growth factor-β (TGFβ) signaling, where TGFβ induces its membrane receptors to directly activate Smad proteins.  These activated Smads complex with Smad4 (co-Smad), translocate from cytoplasm into nucleus and bind to target promoter region to regulate gene transcriptions.  Dysfunction in TGFβ pathway leads to immunosuppression and angiogenesis, which can make cancer more invasive.  

​

Signosis has developed SMAD/TGFb luciferase reporter stable cell lines by co-transfecting a SMAD luciferase reporter vector and a hygromycin expression vector.  The hygromycin resistant clones were subsequently screened for TGFb1-induced luciferase activity.   The cell line can be used as a reporter system for monitoring the activation of SMAD triggered by stimuli treatment, such as TGFb1 and TGFb3, and gene overexpression and gene knockdown.