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PIK3R1 — TGFB1
Text-mined interactions from Literome
Higaki et al., Arterioscler Thromb Vasc Biol 1999
:
We also found that
transforming growth factor-beta stimulated
PI3K activity and the phosphorylation of Akt, a downstream signaling molecule of PI3K
Kang et al., Dev Dyn 2002
:
Phosphatidylinositol-3 (PI-3) kinase regulates cytoskeleton reorganization, cell migration, and
transforming growth factor ( TGF ) beta regulated EMT
Zhu et al., Neuroscience 2004
(MAP Kinase Signaling System) :
Of note, wortmannin and U0126, as well as kappabeta-decoy DNA, abolished the anti-apoptotic effect of TGF-beta1, corroborating the notion that both
PI3k/Akt and MAPK/Erk1,2 pathways, and NF-kappabeta activity are
necessary for the anti-apoptotic activity of
TGF-beta1
Yeh et al., Biochem Pharmacol 2008
(Chondrosarcoma) :
Taken together, these results suggest that the
TGF-beta1 acts through
PI3K/Akt , which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of alphavbeta3 integrins and contributing the migration of chondrosarcoma cells
Kulasekaran et al., Am J Respir Cell Mol Biol 2009
(Idiopathic Pulmonary Fibrosis) :
In this study, we show that, although TGF-beta1 induces fibroblast synthesis and secretion of ET-1,
TGF-beta1 activation of
PI3K/AKT is not dependent on ET-1
Mohamed et al., Am J Physiol Lung Cell Mol Physiol 2010
:
Interestingly, selective inhibitors of PTK,
PI3K , or MEK1/2
attenuated TGF-beta1 expression through blocking ERK1/2 phosphorylation and TGF-beta1 promoter activity in response to stretch