Gene interactions and pathways from curated databases and text-mining

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AKT3 — LPA

Text-mined interactions from Literome

Sautin et al., Am J Physiol Cell Physiol 2001 : LPA stimulated phosphorylation of Akt in a time dependent manner in both intact and toxin treated AML12 hepatocytes
Kou et al., Biochemistry 2002 : In contrast to the cellular responses elicited by S1P in COS-7 cells, LPA can stimulate the activation of eNOS and Akt independently of EDG-1 receptor transfection
Baudhuin et al., Mol Pharmacol 2002 : We show for the first time, with the use of both pharmacological and genetic inhibitors, that the kinase activity and S473 phosphorylation of Akt induced by LPA and S1P requires both mitogen activated protein ( MAP ) kinase kinase ( MEK ) and p38 MAP kinase, and MEK is likely to be upstream of p38, in HEY ovarian cancer cells ... In contrast to S1P and PDGF, LPA requires Rho for Akt S473 phosphorylation, and Rho is upstream of phosphatidylinositol 3-kinase (PI3-K) ... LPA/S1P induced Akt activation may be involved in cell survival, because LPA and S1P treatment in HEY ovarian cancer cells results in a decrease in paclitaxel induced caspase-3 activity in a PI3-K/MEK/p38 dependent manner
Lee-Kwon et al., J Biol Chem 2003 : LY294002 completely prevented the LPA induced increase in Akt phosphorylation, which is consistent with the inhibitory effect of LY294002 on the LPA stimulation of NHE3 activity ... The LPA induced phosphorylation of Akt was the same in OK cells with and without E3KARP
Kam et al., FASEB J 2004 : LPA caused much less phosphorylation of Akt and this was dependent on PLD activity ... Toxin B, which inactivates Rho GTPases, markedly impaired PLD1 activation and phosphorylation of Akt , p70 ( S6K ), and 4E-BP1 induced by LPA but had a minimal or no effect on the actions of PDGF
Hu et al., J Biol Chem 2005 (Leukemia, Lymphocytic, Chronic, B-Cell) : Lysophosphatidic acid (LPA) protects primary chronic lymphocytic leukemia cells from apoptosis through LPA receptor activation of the anti-apoptotic protein AKT/PKB
Yun et al., Am J Physiol Cell Physiol 2005 (Colonic Neoplasms) : LPA2 activated Akt and Erk1/2 in response to LPA
Shah et al., J Cell Physiol 2006 (MAP Kinase Signaling System) : In C9 hepatocytes, agonist activation of AT1 angiotensin II ( AT1-R ), lysophosphatidic acid (LPA) , and EGF receptors caused phosphorylation of Akt through activation of the EGF-R in a PI3K dependent manner
Shah et al., Mol Endocrinol 2005 : In cultured bovine adrenal glomerulosa cells, LPA , which is predominantly coupled to Gi and partially to Gq/protein kinase C alpha and epsilon, caused phosphorylation of Src ( at Tyr416 ), proline-rich tyrosine kinase ( Pyk2 at Tyr402 ), EGF-R, protein kinase B/Akt , extracellularly regulated signal kinases 1/2, and their dependent protein, p90 ribosomal S6 kinase
Baldini et al., Mol Cell Biochem 2005 : Moreover, the LPA induced activation of Akt , a downstream target of PI3K, was completely inhibited by physiological concentrations of ANP, which were also able to inhibit p42/p44 phosphorylation
Stadler et al., Cell Signal 2006 (Breast Neoplasms...) : Further investigations concentrating on cell signalling and motility revealed an abrogation of phosphatidylinositol-3-kinase dependent LPA induced Akt activation and cell migration due to downregulation of the LPA receptor Edg-2 in FGFR4 G388 expressing MDA-MB-231 cells
Jean-Baptiste et al., Biochem Biophys Res Commun 2005 : The demonstration that LPA mediates the activation of ERK1/2 MAP kinase and Akt/PKB in C2C12 cells is consistent with the widely observed mitogenic properties of LPA
Cechin et al., Neurochem Res 2005 (Glioma) : Inhibition of Rho kinase or NHE1 did not reduce the LPA induced phosphorylation of ERK, Akt or CREB
Kim et al., Cell Signal 2006 : GqI expression also attenuated LPA induced ERK1/2 and Akt activation by 40-50 %
Sugimoto et al., Exp Cell Res 2006 : LPA inhibits IGF I-induced Akt activation by only 40 % in a manner dependent on Rho kinase
Zhang et al., Am J Physiol Cell Physiol 2006 : Pertussis toxin ( PTX ) blocks LPA induced activation of p38 and ERK but only slightly inhibits LPA induced activation of Akt
Zhang et al., Cell Signal 2007 : Overexpression of MAGI-3 in SW480 cells showed no apparent effect on LPA induced activation of Erk and Akt
Nebesio et al., Glia 2007 (Disease Models, Animal...) : Furthermore, LPA induced a higher level of Ras-GTP and Akt phosphorylation in Nf1-/- SCs as compared to WT cells
Chen et al., J Cell Biochem 2008 (Hypertrophy...) : In addition, LPA stimulated the phosphorylation of Akt and p65 protein and activated NF-kappaB-luciferase expression
Lee et al., Mol Biol Cell 2008 (Colonic Neoplasms...) : Consistent with negative modulation of the phosphatidylinositol 3 kinase pathway by LPA ( 4 ), LPA ( 4 ) deficiency potentiated Akt and Rac but decreased Rho activation induced by LPA
Ambesi et al., Mol Cancer Res 2009 : Although LPA and S1P activated both PI3K/Akt and Ras/ERK signaling through G ( i ), anastellin inhibited only the Ras/ERK pathway
Malchinkhuu et al., Mol Biol Cell 2009 (Glioma) : The expression of tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 ( PTEN ) is required for the inhibitory ISO induced and Rap1B mediated actions on the migration, Rac1 activation, and Akt activation in response to LPA
Saunders et al., Free Radic Biol Med 2010 (Ovarian Neoplasms) : Exogenous LPA further stimulated ERK and Akt phosphorylation and NF-?B activity
Hooks et al., Molecular cancer 2010 (Ovarian Neoplasms) : We further show that AKT activation is higher following RGS10 knock-down and RGS 10 and RGS17 overexpression blocked LPA mediated activation of AKT , suggesting that RGS proteins may blunt AKT survival pathways
Riaz et al., PloS one 2012 : RICTOR-mTOR was required also for LPA induced AKT Ser473 phosphorylation in MCF7 cells, but, interestingly, not in HeLa cells ... PAK was needed for the AKT Ser473 phosphorylation in response to LPA and PDGF, but not to EGF
Kim et al., Exp Mol Med 2012 (Neoplasms) : Lysophosphatidic acid (LPA)- induced migration was higher than that of epidermal growth factor (EGF) induced migration ; however, LPA induced activation of Akt was lower than that stimulated by EGF
Rai et al., J Exp Med 2012 (Neoplasms) : In vivo, the administration of soluble RAGE or genetic deletion of RAGE mitigated LPA stimulated vascular Akt signaling, autotaxin/LPA-driven phosphorylation of Akt and cyclin D1 in the mammary tissue of transgenic mice vulnerable to carcinogenesis, and ovarian tumor implantation and development
Cho et al., Mol Biol Cell 2013 (Atherosclerosis) : Apo(a) caused the disruption of VE-cadherin/ß-catenin complexes in a Src dependent manner, decreased ß-catenin phosphorylation, and increased phosphorylation of Akt and glycogen synthase kinase-3ß, ultimately resulting in increased nuclear translocation of ß-catenin ; all of these effects are downstream of apo(a) attenuation of phosphatase and tensin homologue deleted on chromosome 10 activity