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AKT1 — SMAD3
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
Song et al., J Biol Chem 2003
:
Insulin-like growth factor-I inhibits transcriptional responses of transforming growth factor-beta by phosphatidylinositol
3-kinase/Akt dependent suppression of the activation of
Smad3 but not Smad2
Remy et al., Nat Cell Biol 2004
:
PKB inhibits
Smad3 by preventing its phosphorylation, binding to Smad4 and nuclear translocation ... In contrast,
Smad3 does not
inhibit PKB
Song et al., EMBO J 2006
:
Novel
roles of
Akt and mTOR in suppressing TGF-beta/ALK5 mediated
Smad3 activation
Horowitz et al., Cell Signal 2007
:
Here, we demonstrate that FAK and
AKT are independently
regulated by early activation of
SMAD3 and p38 MAPK, respectively
Xia et al., American journal of physiology. Renal physiology 2008
(Hyperglycemia) :
In high glucose,
Akt Ser473 phosphorylation appeared within 1 h and
Smad2/3 nuclear translocation was
prevented with neutralizing TGF-beta(1) antibodies
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
Sweetwyne et al., Am J Pathol 2010
:
Collagen stimulation was independent of TGF-ß activity and
Smad phosphorylation but was
blocked by an
Akt inhibitor, suggesting that signaling through the Akt pathway is important for regulation of collagen through TSP1 binding to calreticulin
Dumaresq-Doiron et al., J Cell Physiol 2012
:
At the molecular level, immature Hyal-1 null mice have decreased mRNA expression of follistatin and higher levels of
phospho-Smad3 protein, resulting in increased
levels of
phospho-Akt in pubertal mice
Suwanabol et al., Am J Physiol Heart Circ Physiol 2012
(Carotid Artery Injuries) :
Overexpression of
Smad3 enhanced p38 phosphorylation and inhibition of p38 with a chemical inhibitor or a small interfering RNA
blocked TGF-ß induced
Akt phosphorylation ... Our findings were confirmed in vivo where overexpression of
Smad3 in a rat carotid injury model
led to enhancement of p-p38,
p-Akt , as well as SMC proliferation
Winbanks et al., J Cell Biol 2012
(Hypertrophy) :
Expression of constitutively active
Smad3 not only markedly prevented skeletal muscle growth induced by follistatin but also potently
suppressed follistatin induced
Akt/mTOR/S6K signaling
Han et al., Int J Biochem Cell Biol 2013
:
In addition,
Smad activation inhibits muscle protein synthesis by
suppressing Akt signaling