Gene interactions and pathways from curated databases and text-mining

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AKT3 — CAV1

Text-mined interactions from Literome

Sedding et al., Circ Res 2005 : Furthermore, caveolin-1 is essential for the integrin mediated activation of PI3-K/Akt
Oh et al., J Cell Biochem 2006 : However in contrast to adipocytes, phosphorylation of insulin receptor beta (IRbeta) and Akt/Erk was not affected by the respective downregulation of caveolin-1 or caveolin-3 in the muscle cells
Zhang et al., Cell Signal 2007 : Caveolin-1 phosphorylation is required for stretch induced EGFR and Akt activation in mesangial cells
Albinsson et al., Am J Physiol Cell Physiol 2008 (Hypertrophy...) : In conclusion, caveolin 1 contributes to low basal ERK1/2 and Akt activity and is required for Akt dependent signals in response to shear stress ( flow ) but is not essential for trophic effects of stretch ( pressure ) in the vascular wall
Salani et al., Endocrinology 2008 : These results demonstrate that : 1 ) Cav-1 down-regulation negatively affects IGF-IR tyrosine phosphorylation ; 2 ) this effect causes a reduced activation of insulin receptor substrate-1, Shc, and Akt ; and 3 ) Cav-1 is involved in IGF-IR antiapoptotic signaling after serum deprivation
Di Vizio et al., Cell cycle (Georgetown, Tex.) 2008 (Prostatic Neoplasms) : When overexpressed in Cav-1 negative PCa cells, Cav-1 ( C133/143/156S ) caused a reduction of both Src and Akt levels, as well as of their active, phosphorylated forms, in comparison with wild type Cav-1
Tian et al., J Biol Chem 2009 : Mechanistically, both Src and caveolin-1 are required for ouabain induced activation of Akt and up-regulation of Na/K-ATPase
Park et al., Am J Physiol Cell Physiol 2009 : Especially, phosphorylation of caveolin-1 is attenuated by AG1478, herbimycin A ( tyrosine kinase inhibitors ), and pyrazolopyrimidine 2 ( PP2, Src inhibitor ) and EGF induced ERK activation was blocked by PP2, methyl-beta-cyclodextrin ( MbetaCD ), caveolin-1 small interfering RNA ( siRNA ), LY-294002 [ phosphoinositol-3 kinase inhibitor ( PI3K ) ], and Akt inhibitor
Xia et al., Am J Pathol 2010 (Idiopathic Pulmonary Fibrosis) : We demonstrate that caveolin-1 expression is low in IPF fibroblasts and that this correlates with low membrane PTEN levels, whereas overexpression of caveolin-1 restores membrane PTEN levels, inhibits Akt phosphorylation, and suppresses proliferation
Liao et al., Endocrinology 2010 : Caveolin-1 down-regulation suppressed VEGF stimulated phosphorylation of Akt , JNK, eNOS, c-Src, and FAK ; however, basal activities of c-Src and FAK were elevated in parallel with increased stress fiber formation and focal adhesion ... Caveolin-1 overexpression also inhibited VEGF induced phosphorylation of Akt , JNK, c-Src, FAK, and eNOS
Meyer et al., J Hepatol 2011 : In contrast, non-Smad/AKT pathway activation required functional dynamin mediated endocytosis and the presence of caveolin-1 , an essential protein for caveolae formation
Huang et al., FASEB J 2011 : Exposure to HIV-1 infected monocytes induced phosphorylation of ERK1/2 and Akt in hCMEC by 2.5- and 3.6-fold, respectively ; however, these effects were attenuated by overexpression of PPARa or PPAR? and by silencing of caveolin-1 ( cav-1 )
Basu Roy et al., Int J Cancer 2013 (Cell Transformation, Neoplastic...) : Increased AKT signaling induces caveolin-1 expression by increasing the activity of the transcription factor, Sp1
Yang et al., PloS one 2013 : Furthermore, addition of AGEs enhanced the interaction of phospho-Cav-1 with IGF-1Rß and transfection of 3T3-L1 cells with Cav-1 Y14F mutants inhibited the activation of Akt by AGEs
Nho et al., PloS one 2013 (Idiopathic Pulmonary Fibrosis) : We demonstrate that PTEN over-expression or Akt inhibition increases FoxO3a expression in IPF fibroblasts, resulting in up-regulation of caveolin-1
Ayala et al., J Pathol 2013 (Adenocarcinoma...) : Silencing of Cav-1 by shRNA in WPMY-1 prostate fibroblasts resulted in up-regulation of Akt phosphorylation, and significantly altered expression of genes involved in angiogenesis, invasion, and metastasis, including a? > ?2.5-fold increase in TGF-ß1 and ?-synuclein ( SNCG ) gene expression