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IGFBP3 — SMAD3
Text-mined interactions from Literome
Leal et al., J Biol Chem 1999
:
IGFBP-3 did not
stimulate the cellular phosphorylation of Smad2 and
Smad3 , key transducers of the transforming growth factor-beta type I/type II receptor ( TbetaR-I.TbetaR-II ) heterocomplex mediated signaling
Fanayan et al., J Biol Chem 2000
(Breast Neoplasms) :
Phosphorylation of each
Smad was
stimulated by TGF-beta1 and, independently, by
IGFBP-3 with the two agents together showing a cumulative effect
Fanayan et al., J Biol Chem 2002
(Breast Neoplasms) :
Like TGF-beta1, natural and recombinant
IGFBP-3 stimulated the time- and dose dependent phosphorylation of TGF-betaR1 as well as Smad2 and
Smad3
Ismail et al., Am J Physiol Lung Cell Mol Physiol 2009
:
Smad inhibition does not but the phosphatidylinositol 3-kinase (PI3K) signaling pathway inhibitor LY-294002 does
inhibit NOX4 and
IGFBP-3 gene expression, IGFBP-3 secretion, and cellular proliferation resulting from hypoxia
Zhong et al., J Cell Sci 2011
:
Biochemical assays and in vitro experiments revealed that
IGFBP3 bound BMP2 and
inhibited BMP2 induced
Smad signaling in cultured human cells
de Silva et al., Endocrinology 2012
:
We conclude that
IGFBP-3 activates inhibitory
Smad signaling in 3T3-L1 cells and that endogenous IGFBP-3 modulates their adipogenic differentiation by regulating cell sensitivity towards the inhibitory effect of TGFß