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TGF-β/SMAD2/3/4
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.
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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.