General Information:

Id: 6,785 (click here to show other Interactions for entry)
Diseases: Cancer
Homo sapiens
BTO:0000552 HaCaT cell
article/cited
Reference: Frederick JP et al.(2004) Transforming growth factor beta-mediated transcriptional repression of c-myc is dependent on direct binding of Smad3 to a novel repressive Smad binding element Mol. Cell. Biol. 24: 2546-2559 [PMID: 14993291]

Interaction Information:

Comment TGF-beta initiates its signal through binding the TGF-beta type II serine/threonine (Ser/Thr) receptor kinase, which in turn phosphorylates the type I Ser/Thr receptor, forming an activated receptor complex. The activated type I receptor is then able to phosphorylate its intracellular effector substrates, which include the highly homologous receptor Smads, Smad2 and Smad3 (cited information).
Formal Description
Interaction-ID: 65896

increases_activity of

gene/protein

SMAD2

Drugbank entries Show/Hide entries for SMAD2
Comment TGF-beta initiates its signal through binding the TGF-beta type II serine/threonine (Ser/Thr) receptor kinase, which in turn phosphorylates the type I Ser/Thr receptor, forming an activated receptor complex. The activated type I receptor is then able to phosphorylate its intracellular effector substrates, which include the highly homologous receptor Smads, Smad2 and Smad3 (cited information).
Formal Description
Interaction-ID: 65898

increases_activity of

gene/protein

SMAD3