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PIK3R1 — SMAD2
Text-mined interactions from Literome
Dupont et al., Biol Reprod 2003
:
Using specific inhibitors, we demonstrated that the
activation of
Smad-2 was partially blocked by the inhibition of
PI3K but not by the inhibition of ERK1/2 or p38, suggesting a cross-talk between the Smad and PI3K/Akt pathways
Lee et al., Biochem Biophys Res Commun 2004
:
In addition,
PI3K inhibitor, dominant negative Akt, and dominant negative ILK could not
block TGFbeta mediated C-terminal phosphorylation of
Smad2
Qiao et al., Cancer Lett 2006
(Neuroblastoma) :
GRP induced activation of
PI3-K , resulting in neuroblastoma cell growth promotion, is
potentiated by down-regulation of
TGF-beta/Smad signaling
Sun et al., Cytokine 2006
:
Furthermore, both the PI3K inhibitor LY294002 and the dominant negative AKT ( DN-AKT ) abolished the inhibitory effects of insulin, demonstrating that the inhibition of
Smad2 activation by insulin was
PI3K/AKT dependent
Graham et al., Prostate 2009
(Neoplasm Metastasis...) :
PI3K/Akt dependent transcriptional regulation and activation of
BMP-2-Smad signaling by NF-kappaB in metastatic prostate cancer cells
Heger et al., J Cell Physiol 2010
(Cardiomegaly...) :
Specific inhibitors of
PI3K ( 10 microM LY290042 or 10 nM wortmannin ) or ERK ( 10 microM PD98059 ) also
blocked GDF15 induced hypertrophy and
SMAD activation
Veillette et al., Biol Reprod 2013
:
PI3-K inhibition in vivo blocked Akt phosphorylation,
reduced Smad2 phosphorylation, and reduced both TGF-beta2 and XIAP expression