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PIK3CA — 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