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APOB — SMAD3

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: APOB — SMAD3 (direct interaction, two hybrid) Wang et al., Molecular systems biology 2011
• IRef Intact Interaction: APOB — SMAD3 (physical association, two hybrid) Wang et al., Molecular systems biology 2011

Text-mined interactions from Literome

Song et al., Kidney Int 2005 : These results suggest that Ox-LDL activates TGF-beta/Smad signaling to stimulate PAI-1 transcription in human mesangial cells
Hong et al., Translational research : the journal of laboratory and clinical medicine 2006 : Treatment with PD98059 or UO126, mitogen activated ERK activating kinase 1/2 inhibitors, significantly inhibited the Ox-LDL induced increase in PAI-1 mRNA and nuclear Smad3 expression, DNA/protein complex formation, and PAI-1 promoter activity ... These results suggest that phosphorylation of ERK is induced by Ox-LDL through the induction of the TGF-beta signaling pathway and that activated ERK, in turn, participates in the Ox-LDL induced Smad3 activation and subsequent PAI-1 gene expression in mesangial cells
Song et al., Translational research : the journal of laboratory and clinical medicine 2008 (MAP Kinase Signaling System) : Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity ... Similar to lovastatin, FTI-277, which is an inhibitor of Ras farnesylation, decreased the Ox-LDL induced activation of ERK/Smad3 and induction of TGF-beta1/PAI-1