Gene interactions and pathways from curated databases and text-mining

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SMAD3 — SP1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Biggs et al., J Biol Chem 1999 : Additionally, transfection of Smad3 did not enhance the activation of GAL4/Sp1 by PMA
Poncelet et al., J Biol Chem 2001 : Chemical inhibition of Sp1 binding with mithramycin A, or deletion of the GC boxes, inhibited COL1A2 activation by Smad3 , suggesting cooperation between Smad3 and Sp1 in the TGF-beta1 response ... In a Gal4-LUC reporter assay system, Sp1 stimulated the TGF-beta1 induced transcriptional activity of Gal4-Smad3 , Gal4-Smad4 ( 266 ), or both
Lee et al., Am J Respir Cell Mol Biol 2004 (Cystic Fibrosis) : Analysis of the human SMAD3 promoter demonstrates that isoprenoid regulation of SMAD3 expression is dependent on Sp1/Sp3 activity, although farnesyl mediated pathways may be acting through a secondary mechanism as well
Jungert et al., Carcinogenesis 2006 (Pancreatic Neoplasms) : Moreover, inhibition of Sp1-DNA binding or transfection of Sp1-specific siRNA prevents TGFbeta induced Smad7 expression and consequently enhances Smad signaling in pancreatic cancer cells, as indicated by increased receptor mediated phosphorylation of Smad3
Wang et al., Differentiation 2011 : The increase of Sp1 , but not Smad 2/3 activation was almost completely blocked by the addition of TSA