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AKT1 — 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
Lhuillier et al., J Neurophysiol 2002 : These drugs also inhibit TGFbeta1 effects on Akt/PKB phosphorylation but have no effect on TGFbeta1 evoked Erk activation ... Application of the MEK1 inhibitor PD98059 blocked TGFbeta1 effects on Erk but had no effect on Akt/PKB phosphorylation
Horowitz et al., J Biol Chem 2004 : Pharmacological inhibition of p38 MAPK with SB203580 or expression of a p38 kinase-deficient mutant protein inhibits TGF-beta1 induced PKB/Akt phosphorylation ... Pharmacological inhibition of p38 MAPK with SB203580 or expression of a p38 kinase-deficient mutant protein inhibits TGF-beta1 induced PKB/Akt phosphorylation
Kobayashi et al., J Biol Chem 2004 (Neoplasm Invasiveness...) : Here, we show that 1 ) TGF-beta1 induced a rapid increase of the PI3K activity that was accompanied by increased expression ( 5-fold ) of the uPA mRNA ; 2 ) pharmacological inhibition of PI3K or AS-PI3K ODN transfection inhibited TGF-beta1 stimulated Akt phosphorylation ; 3 ) both PI3K pharmacological inhibitors and forced expression of AS-PI3K ODN reduced TGF-beta1 stimulated uPA mRNA and protein expression by approximately 70 % compared with controls ; 4 ) concentrations of PI3K inhibitors, sufficient to inhibit uPA up-regulation, inhibited TGF-beta1 dependent HRA cell invasion ; 5 ) the AS-PI3K ODN cells had a decreased ability to invade the extracellular matrix layer as compared with controls ; and 6 ) when the AS-PI3K ODN cells were injected intraperitoneally into nude mice, the mice developed smaller intraperitoneal tumors and showed longer survival
Xu et al., Biochem Biophys Res Commun 2003 (Carcinoma, Hepatocellular...) : We found that PKB-Ser-473 phosphorylation was apparently up-regulated by TGF-beta1 ... In the meantime, PKB-Thr-308 phosphorylation was slightly up-regulated by TGF-beta1 ... We first found that TGF-beta1 could stimulate PKB-Ser-473 phosphorylation possibly via up-regulating ILK expression
Tanaka et al., J Biol Chem 2004 (MAP Kinase Signaling System...) : Here, we show that 1 ) nontoxic concentrations of TGF-beta1 activated Src kinase ; 2 ) TGF-beta1 rapidly phosphorylates ERK1/2 and Akt, but not p38 ; 3 ) pharmacological Src inhibitor PP2 or antisense ( AS ) c-Src oligodeoxynucleotide ( ODN ) treatment reduced TGF-beta1 induced phosphorylation of ERK1/2 and Akt by 85-90 % compared with controls ; 4 ) pharmacological inhibition of MAPK by PD98059 abrogated TGF-beta1 mediated Akt stimulation, whereas TGF-beta1 induced ERK1/2 stimulation was not inhibited by PI3K inhibitor LY294002 or AS-PI3K ODN transfection ; 5 ) up-regulation of uPA mRNA in response to TGF-beta1 was almost totally blocked by PP2 and PD98059 and partially ( approximately 55 % ) by LY294002 ; 6 ) TGF-beta1 induced uPA mRNA up-regulation was inhibited by treatment with AS ODNs to c-Src or PI3K by 90 or 60 %, respectively, compared with control ODN treatment ; and 7 ) blockade of the release of the transcription factor NF-kappaB by pyrrolidinedithiocarbamate reduced the TGF-beta1 induced activation of the uPA gene by approximately 65 %
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
Lee et al., Int J Oncol 2004 (Stomach Neoplasms) : In contrast, PKB/Akt regulation by TGF-beta1 was not different in suspension or in adhesion, and Smad7, but not the other Smads, activated PKB/Akt phosphorylation on TGF-beta1 treatment, indicating a specificity of Smad2 mediated and cell adhesion status dependent activation of Erk1/2 activity
Jeong et al., J Cell Biochem 2004 : TGF-beta1 induced phosphorylation of AKT and FAK
Lechuga et al., Am J Physiol Gastrointest Liver Physiol 2004 : Our results also show that this TGF-beta1 mediated effect is de novo protein synthesis dependent and requires the activity of p38MAPK, phosphatidylinositol 3-kinase, AKT , and p70 ( S6k )
Vittal et al., Am J Pathol 2005 (Fibrosis...) : Activation of focal adhesion kinase ( FAK ) and protein kinase B ( PKB/Akt ) by transforming growth factor-beta1 mediate stable induction of myofibroblast differentiation and survival ... In this report, we demonstrate that transforming growth factor-beta1 induced activation of both PKB/Akt and FAK are dose dependently inhibited by the protein kinase inhibitor, AG1879, in cultured human lung fibroblasts ... In this report, we demonstrate that transforming growth factor-beta1 induced activation of both PKB/Akt and FAK are dose dependently inhibited by the protein kinase inhibitor, AG1879, in cultured human lung fibroblasts
Murillo et al., Oncogene 2005 : The activation of c-Src by TGF-beta1 is EGFR dependent and is required for full Akt phosphorylation and cell survival
Shooner et al., Reproductive biology and endocrinology : RB&E 2005 : Moreover, TGF-beta1 reduced both Akt ( a well known survival factor ) phosphorylation and XIAP ( X-linked inhibitor of apoptosis protein ) expression in decidual endometrial stromal cells in vitro
Inagaki et al., J Biol Chem 2005 : Here, we show that 1 ) KTI suppressed TGF-beta1 induced phosphorylation of Src, ERK1/2, and Akt by 40-60 % ; 2 ) KTI was insensitive to suppress the phosphorylation of ERK1/2 and Akt in the constitutively active ( CA ) -c-Src ( Y529F ) cells ; 3 ) uPA expression was up-regulated in TGF-beta1 stimulated HRA cells and in unstimulated Y529F cells ; 4 ) the addition of KTI reduced the TGF-beta1 induced increase of uPA gene and protein expression in the wild-type c-Src transfected cells ( in contrast, KTI could not inhibit uPA expression in the Y529F cells ) ; and 5 ) CA-c-Src transfection resulted in a 2-fold increase in invasiveness, whereas KTI did not reduce invasion of the Y529F cells
Suzuki et al., J Biol Chem 2005 (Anoxia) : AMPK-alpha, Akt, and ARK5 were activated by TGF-beta1 , and Akt and AMPK-alpha phosphorylation, which was prolonged by hypoxia, was suppressed by an inhibitor of type I TGF-beta receptor
Horowitz et al., Am J Physiol Lung Cell Mol Physiol 2006 (Respiratory Distress Syndrome, Adult) : Exogenous transforming growth factor-beta1 markedly induces PKB/Akt activation in AMCs from ARDS-R ... Exogenous transforming growth factor-beta1 markedly induces PKB/Akt activation in AMCs from ARDS-R
Lien et al., Cell Signal 2006 : Phosphatidylinositol 3-kinase/Akt pathway is involved in transforming growth factor-beta1 induced phenotypic modulation of 10T1/2 cells to smooth muscle cells
Horowitz et al., Cell Signal 2007 : Combinatorial activation of FAK and AKT by transforming growth factor-beta1 confers an anoikis-resistant phenotype to myofibroblasts
Lin et al., Eur J Pharmacol 2007 : Stimulation of cells with TGF-beta1 caused an increase in Akt phosphorylation in a time dependent manner, which was inhibited by wortmannin and LY 294002 ( PI3K inhibitors )
Kang et al., J Exp Med 2007 (Pulmonary Fibrosis) : TGF-beta(1) and bleomycin also activated phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB)/AKT via SEMA 7A-dependent mechanisms, and PKB/AKT inhibition diminished TGF-beta(1) induced fibrosis ... TGF-beta(1) and bleomycin also activated phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB)/AKT via SEMA 7A-dependent mechanisms, and PKB/AKT inhibition diminished TGF-beta(1) induced fibrosis
Wang et al., Biochem Biophys Res Commun 2008 : Meanwhile, TGF-beta1 stimulated the phosphorylation of Akt and extracellular signal regulated kinase 1/2 ( ERK1/2 )
Lee et al., American journal of physiology. Renal physiology 2008 : In this study, we aimed to determine whether the sevoflurane mediated phosphorylation of ERK and Akt , induction of HSP70, and reduction in NF-kappaB activation are due to TGF-beta1 receptor mediated signaling after PS externalization in HK-2 cells
Wei et al., Mol Carcinog 2008 (Breast Neoplasms) : Taken together, these results suggest that the osteoblast derived TGF-beta1 acts through Akt and ERK, which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of beta1 and beta3 integrins and contributing the migration of breast cancer cell
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
Kim et al., Cell Signal 2008 : In addition, our results also showed that TGF-beta1 treatment increased the phosphorylation of Akt, and Ad-cav-1 infection augmented this TGF-beta1 induced phosphorylation of Akt
Kattla et al., American journal of physiology. Renal physiology 2008 (Diabetes Mellitus, Experimental...) : Furthermore, overexpression of PTEN, the lipid phosphatase regulator of PKB/Akt activation, inhibited TGF-beta1 induced PKB/Akt activation ... Furthermore, overexpression of PTEN, the lipid phosphatase regulator of PKB/Akt activation, inhibited TGF-beta1 induced PKB/Akt activation
Wang et al., Mol Cell Biol 2008 (Breast Neoplasms) : In HER2 overexpressing mammary epithelial cells, transforming growth factor beta ( TGF-beta ) activated phosphatidylinositol-3 kinase (PI3K)/Akt and enhanced survival and migration
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
Wu et al., J Am Soc Nephrol 2009 (Diabetes Mellitus, Experimental...) : PKC is known to mediate glucose induced TGF-beta1 upregulation through the transcription factor AP-1 ; here, inhibitors of phosphoinositide-3-OH kinase, PKC-beta and Akt, and dominant negative Akt all prevented glucose induced activation of AP-1 and upregulation of TGF-beta1 ... In conclusion, PKC-beta1 is an Akt S473 kinase in glucose treated mesangial cells, and TGF-beta1 transcriptional upregulation requires EGFR/PKC-beta1/Akt signaling
Li et al., J Am Soc Nephrol 2009 (Disease Models, Animal...) : Pharmacologic inhibition of ILK with small-molecule inhibitor QLT-0267 abolished TGF-beta1 induced phosphorylation of Akt and glycogen synthase kinase-3beta, suppressed cyclin D1 expression, and largely restored the expression of E-cadherin and zonula occludens 1
Shyu et al., Eur J Heart Fail 2010 (MAP Kinase Signaling System) : TGF-beta1 induced phosphorylation of PI-3 kinase and Akt, while atorvastatin and wortmannin and Akt inhibitor X inhibited the phosphorylation of PI-3 kinase and Akt induced by TGF-beta1
Kwon et al., J Endod 2010 : However, TGFbeta1 did not affect Akt/NF-kappaB signaling to regulate the migration of MDPC-23 cells