SMAD3 is a direct mediator of transcriptional activation by the TGFβ receptor. The activity of SMAD3 is regulated by the TGFβ receptors, and SMAD3 is phosphorylated and associated with the ligand-bound receptor complex. TGFβ stimulation leads to phosphorylation and activation of SMAD3, which form a complex with SMAD4 that accumulate in the nucleus and regulate transcription of target genes such as CDK inhibitor. SMAD3 containing a C-terminal truncation acts as a dominant-negative inhibitor of the normal TGFβ response. SMAD3 is a major physiologic substrate of the G1 cyclin-dependent kinases CDK4 and CDK2.
after opening, aliquot into smaller quantities and store at -70 °C. Avoid repeating handling and multiple freeze/thaw cycles
Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Transforming growth factor (TGF)-beta stimulation leads to phosphorylation and activation of Smad2 and Smad3, which form complexes with Smad4 that accumulate in the nucleus and regulate transcription of target genes. Here we demonstrate that, following TGF-beta stimulation of epithelial cells
Transforming growth factor-beta (TGF-beta) potently inhibits cell cycle progression at the G1 phase. Smad3 has a key function in mediating the TGF-beta growth-inhibitory response. Here we show that Smad3 is a major physiological substrate of the G1 cyclin-dependent kinases CDK4
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