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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 HepG2 stable cell line by co-transfecting SMAD luciferase reporter vector and 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 over expression and gene knockdown.



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