◀ Back to AKT1

AKT1 — CTGF

Text-mined interactions from Literome

Suzuma et al., J Biol Chem 2000 : Furthermore, overexpression of constitutive active Akt was sufficient to induce CTGF gene expression, and inhibition of Akt activation by overexpressing dominant negative mutant of Akt abolished the VEGF induced CTGF expression
Wu et al., Kidney Int 2006 : CTGF enhanced the mRNA expression and protein release of fractalkine, MCP-1, and RANTES, the expression of phospho ( P ) -p42/44 mitogen activated protein kinase ( MAPK ), P-phosphoinositide 3-kinase (PI3-K), P-Akt , and activity of nuclear factor-kappaB (NF-kappaB) in mesangial cells ... P-PI3-K blockade downregulated the CTGF stimulated expression of P-PI3-K, P-Akt , and NF-kappaB but not P-p42/44 MAPK, and partially decreased the release of the above chemokines ... LXA ( 4 ) dose-dependently inhibited the CTGF stimulated mRNA expression and protein release of the above chemokines, and the expression of P-p42/44MAPK, P-PI3-K, P-Akt , and NF-kappaB
Chien et al., Mol Cancer Res 2006 (Carcinoma, Non-Small-Cell Lung...) : Most interestingly, overexpression of CTGF suppressed insulin-like growth factor-I dependent Akt phosphorylation and epidermal growth factor dependent extracellular signal regulated kinase 1/2 phosphorylation
Hayata et al., Biochem Biophys Res Commun 2008 (Cardiomegaly) : Connective tissue growth factor induces cardiac hypertrophy through Akt signaling
Samarin et al., Mol Cancer Res 2009 : Activation of FoxO transcription factors by inhibition of phosphatidylinositol 3-kinase/AKT signaling resulted in a synergistic increase in CA-4P mediated CTGF induction
Li et al., Phytomedicine 2010 (Hyperplasia) : Furthermore, the augmented expression of CTGF and TIMP-2 in HG-exposed cells was mediated by Akt activation and TGF-beta/Smad signaling through PKCbeta2-responsive signaling pathways
Meyer et al., J Hepatol 2011 : Endocytosis inhibition increased canonical Smad signaling and culminated in a superinduction of Id1 and Smad7 expression, whereas caveolin-1 mediated AKT pathway activation was required for maximal CTGF induction
Zhen et al., PloS one 2013 : Mechanistic analysis revealed that CTGF suppression activated FAK/PI3K/AKT and its downstream signals regulating the cell cycle, epithelial-mesenchymal transition (EMT) and MMPs