◀ Back to MTOR

AKT3 — PIK3R1

Pathways - manually collected, often from reviews:

• KEGG Apoptosis: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, indirect effect)
• KEGG VEGF signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Osteoclast differentiation: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, activation)
• KEGG Focal adhesion: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Jak-STAT signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, phosphorylation)
• KEGG T cell receptor signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG B cell receptor signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein)
• KEGG Fc gamma R-mediated phagocytosis: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Neurotrophin signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Cholinergic synapse: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, activation)
• KEGG Chagas disease (American trypanosomiasis): PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Measles: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Influenza A: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG ErbB signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Colorectal cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, activation)
• KEGG Renal cell carcinoma: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, indirect effect)
• KEGG Prostate cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Melanoma: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Chronic myeloid leukemia: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Acute myeloid leukemia: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Small cell lung cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Non-small cell lung cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• KEGG Chemokine signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
• WikiPathways Regulation of toll-like receptor signaling pathway: PIK3R5/PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3 → AKT3/AKT1/AKT2 (activation)
• WikiPathways Toll-like Receptor Signaling Pathway: PIK3R5/PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3 → AKT3/AKT1/AKT2 (activation)
• WikiPathways Chemokine signaling pathway: PIK3CA/PIK3CD/PIK3R1/PIK3R2/PIK3R3/PIK3CG/PIK3R5/PIK3CB → AKT1/AKT2/AKT3 (activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• STRING interaction: AKT3 — PIK3R1 (interaction, mapped from kegg_pathways)
• STRING interaction: AKT3 — PIK3R1 (interaction, mapped from kegg_pathways)
• STRING interaction: AKT3 — PIK3R1 (interaction, mapped from kegg_pathways)
• STRING interaction: PIK3R1 — AKT3 (interaction, mapped from kegg_pathways)
• STRING interaction: PIK3R1 — AKT3 (interaction, mapped from kegg_pathways)
• STRING interaction: PIK3R1 — AKT3 (interaction, mapped from kegg_pathways)

Text-mined interactions from Literome

Debiais et al., Exp Cell Res 2004 : FGF-2 increased PI3K activity but did not induce phosphorylation of Akt or the downstream effector p70 S6 kinase
Wang et al., Hepatology 2010 (Carcinoma, Hepatocellular...) : The role of the Oct4-AKT-ABCG2 axis in cancer cell chemoresistant machinery suggests that AKT pathway inhibition ( PI3K inhibitors ) not only inhibits cancer cell proliferation, but may also enhance chemosensitivity by target potential chemoresistant cells
Lee et al., J Cell Biochem 2012 (Chondrosarcoma) : The phosphatidylinositol 3-kinase (PI3K), Akt , and NF-?B pathways were activated by MIF treatment, and the MIF induced expression of integrin and migration activity were inhibited by the specific inhibitors and mutant forms of PI3K , Akt, and NF-?B cascades
Faghiri et al., Exp Eye Res 2010 : Inhibition of PI3K or mTOR/p70S6K by wortmannin and rapamycin, respectively, increased apoptosis and inhibited phosphorylation of Akt and p70S6K induced by single-dose oxidative stress
Hou et al., J Neurosci 2004 : Two structurally unrelated PI3K inhibitors, LY294002 and wortmannin, blocked the DHPG induced increases in phosphorylation of Akt and mTOR
Goetze et al., Biochem Biophys Res Commun 2001 : Thus, TNFalpha selectively interferes with insulin 's antiapoptotic signaling in VSMC by inhibiting the association of IRS-1/PI3K and the downstream activation of Akt
Lei et al., Am J Physiol Lung Cell Mol Physiol 2011 : In the present study, we assessed the role of Akt in Na-K-ATPase activity and the interaction between the PI3K and MAPK in response to T3 by using MP48 cells, inhibitors, and constitutively active mutants in the MP48 ( alveolar type II-like ) cell line
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
Chung et al., Endocr J 2011 : In addition, phospho-Akt was translocated to the nucleus in response to ghrelin and PI3K inhibition by LY294002 prevented ghrelin induced effect on phospho-Akt localization
Kihara et al., Biochem Biophys Res Commun 2004 : Galantamine induced phosphorylation of Akt , an effector of phosphatidylinositol 3-kinase (PI3K), while PI3K inhibitors blocked the protective effect and Akt phosphorylation
Brown et al., Infect Immun 2011 (Colitis...) : We show that the inhibition of PI3K signaling attenuates epithelial Akt activation, the Ser552 phosphorylation and activation of ß-catenin, and epithelial cell proliferative responses during C. rodentium infection
Huang et al., Pharm Biol 2013 (Disease Models, Animal...) : PI3K inhibitor wortmannin not only blocked catalpol induced Akt activation, but also attenuated all the beneficial effects of catalpol
Ohsawa et al., Glia 2007 : ATP stimulation increased Akt phosphorylation in the microglia, and the increase was reduced by the PI3K inhibitors and a P2Y ( 12 ) R antagonist
Shukla et al., Int J Cancer 2007 (Neoplasm Invasiveness...) : Immunoblot analysis of PI3K and total/activated levels of Akt showed increased protein levels of catalytic ( p110alpha/beta ) and regulatory ( p85 ) subunits of PI3K and constitutive Akt activation in high-grade tumors compared to low-grade tumor and benign tissue
Choi et al., Biofactors 2012 : Honokiol and magnolol stimulate glucose uptake by activating PI3K dependent Akt in L6 myotubes
Varma et al., Am J Physiol Heart Circ Physiol 2005 (Hyperglycemia) : We conclude that d-glucose regulates Akt signaling through threonine phosphorylation of Akt and that hyperglycemia impaired PI3k-Akt signaling may promote EC proliferative dysfunction in diabetes
Lee et al., Am J Physiol Heart Circ Physiol 2006 (Inflammation...) : The PI3K inhibitor and a dominant negative mutant of Akt suppressed Akt and eNOS phosphorylation and NO production
Toulany et al., Mol Cancer Res 2007 (Neoplasms) : These results indicate that PI3K mediated activation of AKT in K-RASmt human tumor cells as a function of EGFR ligand or radiation stimulus is independent of a direct function of K-Ras enzyme activity but depends on a K-Ras mediated enhanced production of EGFR ligands ( i.e., most likely AREG ) through up-regulated extracellular signal regulated kinase-1/2 signaling
Guo et al., J Biol Chem 2011 (Breast Neoplasms...) : IKBKE activation of Akt was not affected by inhibition of PI3K , knockdown of PDK1 or mTORC2 complex
Shenoy et al., J Immunol 2003 : The time courses for phosphorylation and translocation of the p85 subunit of class I ( A ) PI3K , activation of Akt , and activation of PKCzeta were similar
Martin et al., Cancer Res 2011 (Colorectal Neoplasms) : Although AKT activity was elevated in KRAS mutant cells, and PI3K inhibition did impair the growth of MEK inhibitor-insensitive CRC cell lines, concurrent treatment with selumetinib did not provide additional antitumor activity
Bruning , Anticancer Agents Med Chem 2013 : Inhibition of the mTOR signaling pathway by quercetin has directly been described and can further be deduced from its interference with PI3K dependent Akt stimulation, AMP dependent protein kinase activation and hamartin upregulation
Gao et al., Toxicol Appl Pharmacol 2010 : A constitutive level of PI3K dependent Akt phosphorylation remained unchanged by Ni and/or MALP-2 exposure
Kim et al., Exp Mol Med 2009 : A chemical inhibitor of MEK1/2 or PI3K reduced phosphorylation of ERK or Akt , respectively, and also inhibited CSE mediated MMP-9 induction
Raufman et al., J Cell Physiol 2008 (Colonic Neoplasms) : Both EGFR kinase and PI3K inhibitors attenuated DCT induced Akt phosphorylation and Akt activation, as demonstrated by reduced phosphorylation of a GSK-3-paramyosin substrate
Vantler et al., FEBS Lett 2006 : Characterization of the downstream signaling events revealed that PI3K activates the protein kinase Akt , which in turn phosphorylates and thus inactivates proapoptotic Forkhead transcription factors
Zhan et al., Biochem Biophys Res Commun 2004 (Leukemia, Megakaryoblastic, Acute) : Phosphorylation of Akt at serine 473 and its downstream molecular Bad at serine 136 was induced by HAPO, but was blocked by two PI3K inhibitors, LY294002 and wortmannin
Park et al., J Immunol 2003 : Upon treating with group IIA PLA(2), Akt is phosphorylated in a PI3K dependent manner
Kandasamy et al., Cancer Res 2002 (Carcinoma, Non-Small-Cell Lung...) : Furthermore, the loss of PTEN activity or overexpression of PI3-K dependent Akt/protein kinase B activity promotes the survival of NSCLC cells
Sury et al., Neurobiol Dis 2011 (Disease Models, Animal...) : Protein levels and activity of PTEN, the major antagonist of PI3K, were unaltered by infection, suggesting that the observed decrease in PIP ( 3 ) and Akt phosphorylation is a result of decreased PI3K signaling ... These results indicate that the inhibitory effect of bpV ( pic ) on apoptosis was mediated by PI3K dependent activation of Akt , strongly suggesting that bpV ( pic ) acted on PTEN
Ji et al., PloS one 2013 : Moreover, the PI3K inhibitor wortmannin significantly inhibited activation of Akt and AMPK, reduced GLUT4 translocation, glucose uptake and ultimately, depressed IPC induced cardioprotection
Di Segni et al., J Mol Neurosci 2005 : The PI3K signaling pathway might be involved in this effect of NRG as the downstream effector of PI3K, protein kinase B ( PKB/AkT ), is activated by NRG in the presence of Abeta, and PKB/AkT activation is inhibited by the PI3K inhibitor, LY294002
Hennenlotter et al., Oncol Rep 2008 (Carcinoma, Renal Cell...) : We concluded that a strong expression of PTEN in renal cell cancer did not block the PI3K mediated phosphorylation of Akt in the tumour specimens analysed
Liu et al., J Virol 2003 (Cell Transformation, Viral) : Furthermore, the PI3K-specific inhibitor LY294002 could inhibit Akt activation and cell transformation in all cases, indicating that Akt activation and transformation is PI3K dependent
Bai et al., Life Sci 2010 (Carcinoma, Hepatocellular...) : The phosphorylation of EGFR and Akt were elevated in EP1 agonist treated cells, and both EGFR and PI3K inhibitors suppressed the upregulation of survivin induced by PGE ( 2 ) or EP1 agonist
Kim et al., Am J Chin Med 2009 : Only LY294002 inhibited Akt activation induced by EGCG, implying that EGCG induced Akt activation is PI3K dependent
Park et al., Haematologica 2010 (Leukemia, Myeloid, Acute) : However, as mTORC1 activation is independent of PI3K/AKT in acute myeloid leukemia, dual PI3K and mTOR inhibitors may induce apoptosis in blast cells
St-Germain et al., Int J Oncol 2004 (Endometrial Neoplasms) : Inhibition of PI 3-K with Wortmannin and LY294002 blocked Akt phosphorylation and inhibited expression of COX-2 in mutated-PTEN cells
Xu et al., Mol Med Report 2013 : However, LY294002, a PI3K inhibitor, attenuated the anti-apoptotic effect of salidroside and blocked the increase of Akt and mTOR ; however, did not affect the antioxidative effect of salidroside
Gao et al., Am J Physiol Cell Physiol 2004 (Ovarian Neoplasms) : The inhibition of PI3K activity also inhibited the phosphorylation of AKT and p70S6K1, but not extracellular regulated kinase 1/2
Tachado et al., PloS one 2008 : Furthermore, PI3K activation led to Akt stimulation, a serine/threonine kinase, which was also inhibited by wortmannin and LY294002
Cohen et al., Antioxid Redox Signal 2011 (Myocardial Infarction...) : Phosphatidylinositol 3-kinase activation results in phosphorylation of Akt promoting activation of nitric oxide synthase and nitric oxide production, which inhibits glycogen synthase kinase-3ß, perhaps the final cytosolic signaling step before inhibition of MPTP formation
Hunzicker-Dunn et al., Proc Natl Acad Sci U S A 2012 : PI3K activation leads to activation of AKT through phosphorylation of AKT on Thr ( 308 ) and Ser ( 473 )
Goncharova et al., Am J Physiol Lung Cell Mol Physiol 2002 : In parallel experiments, stimulation of human PVSM cells with PDGF induced PI3K dependent activation of Akt , p70 S6 kinase, and ribosomal protein S6 but not mitogen activated protein kinase
King et al., Mol Cell Biol 1997 : Phosphatidylinositol 3-kinase is required for integrin stimulated AKT and Raf-1/mitogen activated protein kinase pathway activation
Preuss et al., Cell Microbiol 2010 : We show that treatment of HEK293 cells with PMT inhibits staurosporine mediated apoptosis through PI3K dependent phosphorylation of Akt and constitutive expression of Pim-1 kinase
Marzec et al., Oncogene 2007 (Lymphoma, T-Cell) : Accordingly, whereas the low-dose PI3K inhibitor wortmannin and Akt inhibitor III profoundly inhibited Akt phosphorylation, they had a very modest effect on S6rp and 4E-BP1 phosphorylation
von Gise et al., Mol Cell Biol 2001 : The survival effect of activated MEK in 32D cells is achieved by both MEK- and PI3K dependent mechanisms and results in the activation of PI3K and in the phosphorylation of AKT
Morrison et al., J Virol 2003 : LMP2A activated Akt in a PI3K dependent manner, and the downstream Akt targets glycogen synthase kinase 3beta ( GSK3beta ) and the Forkhead transcription factor FKHR were phosphorylated and inactivated in LMP2A expressing HFK cells
Li et al., Mol Cell Neurosci 2001 : PI3K inhibitors that blocked NRG mediated rescue also blocked the phosphorylation of Akt , MAPK, and Bad
Xu et al., J Cell Biochem 2008 (MAP Kinase Signaling System) : The activation of ERK1/2 was inhibited by a PI3K inhibitor, LY294002, but U0126, a ERK1/2 inhibitor did not inhibit phosphorylation of Akt and GSK3 beta
Ornelas et al., Int J Dev Neurosci 2010 : Activation of these pathways by ATP seemed to be independent, since LY294002 and U0126, inhibitors of PI3K and MEK, did not block the activation of ERK and AKT , respectively, although each compound blocked its respective target
Quan et al., Exp Parasitol 2013 : The PI3K inhibitors, LY294002 and Wortmannin, both blocked parasite induced phosphorylation of PKB/Akt and Bad
Yoon et al., Biochem Biophys Res Commun 2008 : Pharmacologically blocking PI3K significantly inhibited Akt and GSK3beta phosphorylation
Radhakrishnan et al., J Biol Chem 2008 (MAP Kinase Signaling System) : Cellular exposure to 25 mm glucose, which is required for Shc phosphorylation in response to IGF-I, resulted in enhanced Grb2 binding to p85, activation of PI3K activity, and increased AKT phosphorylation as compared with cells exposed to 5 mm glucose
Suga et al., Arch Biochem Biophys 2005 (MAP Kinase Signaling System) : Furthermore, LY294002 or Akt inhibitor did not affect the AVP induced phosphorylation of p38 MAP kinase and SB203580 did not affect the phosphorylation of PI3K or Akt
Venkatachalam et al., Am J Physiol Heart Circ Physiol 2008 (Hyperglycemia) : HG induces phosphoinositide 3- kinase [PI3K ; inhibited by adenoviral ( Ad ) .dominant negative ( dn ) PI3Kp85 ], Akt ( inhibited by Ad.dnAkt1 ), and ERK ( inhibited by PD-98059 ) activation and induces IL-17 expression via PI3K -- > Akt -- > ERK dependent signaling
Bellis et al., Arterioscler Thromb Vasc Biol 2009 (Disease Models, Animal...) : Late ischemic PC protects BAECs against hypoxia through PKA- and PI3K dependent activation of Akt
Moshal et al., J Cell Physiol 2008 (Hyperhomocysteinemia) : The result suggested that Hcy downregulated CYP2J2 protein expression and dephosphorylated PI3K dependent AKT signal
Lee et al., Development 2007 : Akt was rapidly phosphorylated when GDNF was added to the GS cell culture, and the addition of a chemical inhibitor of PI3K prevented GS cell self-renewal
Uranga et al., Toxicological sciences : an official journal of the Society of Toxicology 2009 : Both Akt and GSK3beta phosphorylation were dependent on PI3K activation
Wygrecka et al., Am J Respir Cell Mol Biol 2012 (Idiopathic Pulmonary Fibrosis) : Exposure of HLFs to TGF-ß1 activated JNK in a PI3K dependent manner and induced Akt phosphorylation at threonine 308 and serine 473, but did not change the phosphorylation status of threonine 450
Feliers et al., Kidney Int 2005 (MAP Kinase Signaling System) : VEGF stimulated Akt phosphorylation in a PI3K dependent manner
Hashimoto et al., Int J Mol Med 2005 : This APJ dependent activation of Akt/PKB was significantly inhibited by the pretreatment of pertussis toxin ( PTx ) and a PI3K inhibitor, LY29004
Zdychová et al., Experimental biology and medicine (Maywood, N.J.) 2008 (Diabetes Mellitus, Type 2...) : Acute PI3K inhibition with wortmannin ( 100 mug/kg ) attenuated renal Akt and mTOR activities in ZO, but not in ZL rats
Mandal et al., Endocrinology 2009 : Together, these data for the first time demonstrate that PI3K dependent Akt activation regulates BMP-2 induced CSF-1 expression and provides a mechanism for osteoblastic cell assisted osteoclast differentiation
Tuo et al., Am J Physiol Cell Physiol 2009 : Forskolin and 8-Br-cGMP not only increased the activity of PI3K but also induced the phosphorylation of Akt , a signaling molecule downstream of PI3K, which were again inhibited by wortmannin and LY294002
Gauthier et al., Am J Physiol Cell Physiol 2001 (MAP Kinase Signaling System) : Herein, we report that 1 ) the enterocytic differentiation process results in the establishment of distinct profiles of Bcl-2 homolog expression levels, as well as p125(Fak), p42 ( Erk-2 ), and p57 ( Akt ) activated levels ; 2 ) the inhibition of Fak, of the MEK/Erk pathway, or of PI3-K, have distinct impacts on enterocytic cell survival in undifferentiated ( subconfluent Caco-2, confluent HIEC-6 ) and differentiated ( 30 days postconfluent Caco-2 ) cells ; 3 ) exposure to insulin and the inhibition of Fak, MEK, and PI3-K resulted in differentiation state-distinct modulations in the expression of each Bcl-2 homolog analyzed ; and 4 ) Fak, beta1 and beta4 integrins, as well as the MEK/Erk and PI3-K/Akt pathways, are distinctively involved in cell survival depending on the state of cell differentiation
Qin et al., Biochemistry 2003 : The activation of Akt , as monitored by its ability to phosphorylate GSK-3alpha/beta and by its S473 phosphorylation, was strictly dependent on PI3K activity
Kim et al., J Neurochem 2013 (MAP Kinase Signaling System) : Immunoblot analysis revealed that PI3K mediated activation of Akt preceded Erk1/2 activation in NRG1ß treated MPG neurons
Sasaki et al., Nature 2000 (Adenocarcinoma...) : PI(3)K mediated activation of the cell survival kinase PKB/Akt , and negative regulation of PI(3)K signalling by the tumour suppressor PTEN ( refs 3, 4 ) are key regulatory events in tumorigenesis
Choi et al., Oncogene 2004 : The specific PI3K inhibitor LY294002 inhibits PI3K/Akt signaling and potentiates the radiation induced apoptosis, suggesting that activation of the PI3K/Akt signaling pathway is involved in the increased radio-resistance in cells overexpressing 12V-Ha-Ras
Duan et al., Biochem Biophys Res Commun 2002 (Breast Neoplasms) : E2 activates constructs containing multiple copies of the SRF ( pSRF ) and a GAL4-SRF fusion protein ; these responses are accompanied by PI3-K dependent phosphorylation of Akt and inhibited by wortmannin/LY294002, the antiestrogen ICI 182780, but not by the mitogen activated protein kinase kinase ( MAPKK ) inhibitor PD98059
Lin et al., Toxicol Appl Pharmacol 2008 : LPS stimulated Src, PYK2, EGFR, and Akt phosphorylation and VCAM-1 expression were attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ), PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110
Chen et al., Cancer Res 2001 (Fibrosarcoma) : Hypoxia induced signaling also resulted in PI 3-K dependent phosphorylation of Akt on Ser-473, a modification of Akt that is important for its activation
Mehta et al., J Immunol 2005 (MAP Kinase Signaling System) : In this report, we show that in intestinal epithelial cells, HB-EGF triggered PI3K dependent phosphorylation of Akt
Mandl et al., Mol Cell Biol 2007 : PI3K dependent activation of Akt is critical for myoblast differentiation induced by serum withdrawal, suggesting that in these cells PI3K signaling is activated in an unconventional manner
Bao et al., Am J Physiol Lung Cell Mol Physiol 2005 : We found that KGF induces a dose- and time dependent increase in Akt kinase activity and that, as expected, activation of Akt via KGF is PI3K dependent
Pijet et al., Cytokine 2013 (MAP Kinase Signaling System) : In contrary, insulin evoked PI3-K dependent phosphorylation of AKT ( S ( 473 ) ) and GSK-3ß ( S ( 9 ) ) and insulin surpassed leptin dependent inhibition of myogenic differentiation in PI3-K dependent manner
Xiao et al., Virology 2009 : The PI3K-speci fi c inhibitor, LY294002, suppressed Akt phosphorylation in a dose dependent manner, suggesting that AcMNPV induced Akt phosphorylation is PI3K dependent
McCubrey et al., Oncogene 2004 (Cell Transformation, Neoplastic...) : MEK or PI3K inhibitors suppressed ERK or Akt activation, respectively, and induced apoptosis in the v-ErbB : ER-responsive cells
Luo et al., J Pharmacol Exp Ther 2007 : The stimulation of Akt phosphorylation was inhibited in a concentration dependent manner by the PI3K inhibitor, 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ( LY294002 )
Di Fulvio et al., Cell Signal 2008 : Transient expression of PLD2 in COS7 cells with either the WT or with a Y179F mutant, resulted in an increased basal phosphorylation of AKT in residues T308 and S473, in a PI3K dependent manner
Sandra et al., Oral Oncol 2004 (Ameloblastoma...) : MK could induce phosphorylation of p44/42 MAPK ( Thr202/Tyr204 ) and Akt ( Ser473 and Thr308 ), and by pretreatment of PD98059, MEK1 inhibitor, or LY294002, PI3K inhibitor, MK-stimulated-phosphorylation of MAPK and Akt and MK-stimulated growth of AM-1 cells were inhibited
Dufour et al., Biochem Biophys Res Commun 2013 (Neoplasms, Experimental) : In particular, PI3K blockade leads to the inhibition of AKT , a major downstream effector responsible for the oncogenic activity of PI3K ... However, we report here that small molecule inhibitors of PI3K only transiently block AKT signaling ... This study shows that PI3K inhibitors only transiently inhibit AKT which limits their antitumor activities
Lankat-Buttgereit et al., Biol Cell 2008 (Diabetes Mellitus, Type 2) : The enhanced secretion of CgA and Sg II seemed to be mediated by an activation of protein kinase Akt via PI3K ( phosphoinositide 3-kinase )
Nadler et al., Am J Physiol Endocrinol Metab 2001 (Insulin Resistance) : Thus BtB6 mice demonstrate the dissociation of insulin stimulated PI3K activity and Akt/PKB activation and represent a useful model to investigate the causes of insulin resistance in humans
Park et al., J Cell Physiol 2011 : In addition, laminin-111 induced Akt phosphorylation was inhibited by integrin ß1 small interfering RNA ( siRNA ) and PI3K inhibitors ( LY294002 and wortmannin )
Wang et al., Am J Physiol Heart Circ Physiol 2010 (Disease Models, Animal...) : Importantly, inhibition of either PI3K or eNOS attenuated exercise induced restoration of the dilatation function and blocked PI3K, Akt , and eNOS phosphorylation by ACh in the mesenteric arteries
Guijarro et al., Carcinogenesis 2007 : Furthermore, activation of AKT by MAP17 as measured by Thr308 phosphorylation was independent of PI3K activity
Gan et al., J Biol Chem 2011 : In HEK293T cells, insulin and constitutively active mutants of small GTPase H-Ras and PI3K could induce HM phosphorylation of both AKT mutants, which was blocked by the PI3K inhibitor LY294002
Zanou et al., J Biol Chem 2012 : Indeed, phosphorylation of both Akt and p70S6K proteins was decreased as well as the activation of PI3K , the main upstream regulator of the Akt
Samoylenko et al., Carcinogenesis 2012 (Adenocarcinoma...) : Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src, Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility
Zhuang et al., Photochem Photobiol 2003 : Thus, activation of Akt by 1O2 is mediated by PI3-K and contributes to a survival response that counteracts cell death after 1O2 induced injury
Huang et al., Acta Pharmacol Sin 2005 (Breast Neoplasms...) : The PI3K inhibitors wortmannin and Ly294002, but not rapamycin, completely inhibited the phosphorylation of Akt and PRAS40
Rodríguez-Escudero et al., J Biol Chem 2009 : Phosphatidylinositol 3-kinase dependent activation of mammalian protein kinase B/Akt in Saccharomyces cerevisiae, an in vivo model for the functional study of Akt mutations
Zhuang et al., J Neurosci 2004 (Hyperalgesia...) : Capsaicin and NGF induce phosphorylation of the PI3K downstream target AKT ( protein kinase B ), which is blocked by the PI3K inhibitors LY294002 and wortmannin, indicative of the activation of PI3K by both agents
Liu et al., Neoplasia (New York, N.Y.) 2008 : On the basis of gene expression array studies, we identified Aurora A as one of the genes regulated transcriptionally by Akt inhibitors including Compound A. Inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, either by PI3K inhibitor LY294002 or by Compound A, dramatically inhibits the promoter activity of Aurora A, whereas the mammalian target of rapamycin inhibitor has little effect, suggesting that Akt might be responsible for up-regulating Aurora A for mitotic progression
Cheng et al., Br J Pharmacol 2012 : Immunoblotting and immunohistochemical studies further showed that inhibition of PI3K significantly blocked renin induced eNOS-Ser 117 and Akt-Ser473 phosphorylation in situ
Haga et al., Endothelium : journal of endothelial cell research 2003 : Phosphorylation of Akt in EC exposed to SS or CS was time dependent but with maximal stimulation at 30 min ( SS ) or 5 min ( CS ) ; SS- or CS-induced Akt phosphorylation was inhibited in the presence of PI3K inhibition
Liu et al., J Immunol 2010 (Inflammation) : Mechanoactivation of VEGFR2 results in its nuclear translocation and elevation of PI3K dependent Ser473-Akt phosphorylation
Hung et al., Stem Cells 2007 : Also, addition of CdM ( Hyp ) activated the PI3K-Akt pathway ; the levels of p-Akt and several of its downstream targets were increased by CdM ( Hyp ), and both the increase in p-Akt and the increase in angiogenesis were blocked by an inhibitor of PI3K-Akt or by expression of a dominant negative gene for PI3K
Hehlgans et al., Int J Radiat Biol 2007 : On the basis of the presented data, a precise correlation of adhesion-, serum- and PI3K mediated changes in PI3K/AKT and FAK/Paxillin/p130Cas signaling cascades was not found
Zhuang et al., American journal of physiology. Renal physiology 2004 : Inhibition of PI3K with LY-294002 blocked Akt phosphorylation and proliferation, whereas U-0126 blocked ERK1/2 phosphorylation but had no effect on proliferation
Robertson et al., Regul Pept 2009 : The increased migration and sprouting of endothelial cells, due to resistin, were blocked by wortmannin ( 100 nM ) and LY294002 ( 10 microM ), inhibitors of phosphatidylinositol-3-kinase (PI3K), and accompanied by PI3K dependent phosphorylation of Akt ; moreover, while the changes were not associated with altered production of nitric oxide ( NO ), resistin induced angiogenic responses were inhibited by IKK Inhibitor X ( 5 microM ), an inhibitor of activation of nuclear factor (NF)-kappaB
Hsu et al., Eur J Pharm Sci 2012 : BBR ( 0.1-10 nM ) led to increasing insulin receptor expression, Akt phosphorylation and enhanced oxidant-sensitive Nrf2/HO-1 induction, which were blocked by a PI3K inhibitor, LY294002
Gentili et al., Biochim Biophys Acta 2003 : The data also indicates a positive role for intracellular calcium in one of the early signals of PTH in rat enterocytes, the activation of PI3K , and that hormone regulation of PI3K activity and Akt/PKB phosphorylation on Thr ( 308 ) is impaired with ageing
Choi et al., J Recept Signal Transduct Res 2004 : In these R- cells, PI3K inhibition by LY294002 enhanced insulin stimulation of ERK phosphorylation whereas LY294002 inhibited insulin stimulation of Akt phosphorylation
Song et al., Cell Signal 2010 : In this study, we report that Src, c-Cbl, and PI3K are involved in the phosphorylation of Akt during TRAIL treatment
Song et al., Journal of neuroinflammation 2012 (Neuroblastoma) : We also found that Src/PI3K/Akt inhibitors prevented LLLT stimulated Akt ( Ser473 and Thr308 ) phosphorylation and blocked Rac1 activity and actin based microglial phagocytosis, indicating the activation of Src/PI3K/Akt/Rac1 signaling pathway
Hirai et al., Brain Res Mol Brain Res 2004 (Anoxia) : PI3K inhibition in neonatal rat brain slices during and after hypoxia reduces phospho-Akt and increases cytosolic cytochrome c and apoptosis
Busch et al., J Biol Chem 2012 : IL-1ß induced NF-?B and PI3K activation was inhibited by resveratrol or the inhibitors of PI3K ( wortmannin ), c-Src ( PP1 ), and Akt ( SH-5 ) through inhibition of I?B kinase, I?Ba phosphorylation, and inhibition of nuclear translocation of NF-?B, suggesting that PI3K signaling pathway may be one of the signaling pathways inhibited by resveratrol to abrogate NF-?B activation
Ozes et al., Nature 1999 : Wortmannin ( a PI(3)K inhibitor ), dominant negative PI(3)K or kinase-dead Akt inhibits TNF mediated NF-kappaB activation
Zhu et al., Kidney Int 2008 : Stable transfection of rat nephrin in the podocytes with podocin led to nephrin tyrosine phosphorylation, PI3K dependent phosphorylation of Akt , increased Rac1 activity, and an altered actin cytoskeleton with decreased stress fibers and increased lamellipodia
Xing et al., Journal of neuroinflammation 2008 (Encephalitis) : Elevations of phosphorylated PPAR-gamma, PI3K, and Akt levels were observed with pioglitazone treatment, and inhibition of PI3K activity enhanced LPS induced NO production
Festuccia et al., Endocr Relat Cancer 2005 (Prostatic Neoplasms) : PI3K inhibition, by LY294002 or after PTEN transfection, restores EGFR stimulated Akt signalling and sensitizes the cells to pro-apoptotic action of gefitinib
Fernandez-Gomez et al., Neurobiol Dis 2006 (Nerve Degeneration) : Moreover, phosphatidylinositol 3-kinase (PI3K) inhibitors attenuated pyruvate induced cytoprotection indicating that PI3K mediated Akt activation is necessary for pyruvate to induce cytoprotection
Song et al., Experimental biology and medicine (Maywood, N.J.) 2008 (Stomach Neoplasms) : Furthermore, PI3-K inhibitor LY294002 attenuated OPN mediated Akt activation
Burnham et al., Microbiology 2007 : Western blot analysis revealed that phosphorylation of host-cell Akt and glycogen synthase kinase-3 ( GSK-3 ) occurs in response to GBS infection, and that this is mediated upstream by PI3K
Chung et al., Biochem Biophys Res Commun 2008 (MAP Kinase Signaling System) : The PI3K inhibitor Wortmannin suppressed icariin mediated angiogenesis and Akt and eNOS activation without affecting ERK phosphorylation
Carricaburu et al., Proc Natl Acad Sci U S A 2003 : PIP4K II beta expression did not impair insulin dependent association of PI3K with insulin receptor substrate 1 (IRS1) but abbreviated Akt activation , indicating that PIP4K II regulates PI-3,4,5-P3 degradation rather than synthesis
Stojanovic et al., J Biol Chem 2006 : Here we show that PI3K mediated Akt activation plays an important role in agonist stimulated platelet NO synthesis and cGMP elevation
Radhakrishnan et al., J Immunol 2007 : Analysis of human or mouse DC treated with the B7-DC cross linking Ab revealed PI3K dependent phosphorylation of AKT accompanied by mobilization of NF-kappaB
Alladina et al., J Vasc Res 2005 : Inhibition of PI3K reduces p-Akt , with concurrent reductions in c-FLIP ( S ) and Bcl-2, and so renders endothelium sensitive to TRAIL induced apoptosis through the extrinsic and intrinsic pathways
Zhou et al., Arterioscler Thromb Vasc Biol 2003 : LY294002, a PI3K inhibitor, and N-acetylcysteine, a scavenger of reactive oxygen species, inhibited the stretch activation of Akt
Datta et al., Cancer Res 2007 (Carcinoma, Hepatocellular...) : Suppression of MT-1 and MT-2A by ectopic expression of the constitutively active PI3K or AKT and their up-regulation by dominant negative PI3K or AKT mutant confirmed negative regulation of MT expression by PI3K/AKT signaling pathway
Liao et al., J Cell Physiol 2011 (Inflammation) : In conclusion, MSF-2 opposes fMLP mediated neutrophil activation and inflammation by inhibiting PI3K activation and subsequent activation of AKT and PLC?2
Gupta et al., Lung 2004 (Carcinoma, Non-Small-Cell Lung...) : Pharmacologically inhibiting PI3K led to decreased Akt phosphorylation and radio sensitization of all three cell lines
Singh et al., Biochem Biophys Res Commun 2005 : Two of the key signalling processes known to be involved in the regulation of cytoskeletal remodelling were investigated : PI(3)K dependent Akt phosphorylation and intracellular calcium concentration [ Ca ( 2+ ) ] ( i )
Peng et al., J Gen Virol 2010 (Herpesviridae Infections) : We found that de novo infection of MHV-68 induced PI3K dependent Akt activation and the lytic replication of MHV-68 was enhanced by inhibiting the PI3K-Akt pathway with both chemical inhibitors and RNA interference technology
Zhang et al., Exp Brain Res 2009 : The importance of the PI3K pathway was further confirmed by the activation of Akt and anti-apoptotic Bcl-2 by cryptotanshinone in a PI3K dependent manner
Xuan Nguyen et al., Biochem Biophys Res Commun 2006 (Prostatic Neoplasms) : Employing the PI3K inhibitor and a variety of mutants PI3K, we showed that nuclear translocation of Akt was mediated by activation of PI3K , and Akt phosphorylation status in the nucleus required PI3K activity ... Thus the activity of PI3K might contribute to the nuclear translocation of Akt , and that Akt phosphorylation is essential for its nuclear retention under NGF stimulation conditions
Wong et al., Biotechnol Bioeng 2006 : The phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin, totally blocked the effect of both zinc and insulin on Akt activation, indicating the involvement of PI3K in the activation of Akt by zinc, rather than zinc acting on Akt directly
Nakagawa et al., Oncol Rep 2007 (Carcinoma, Squamous Cell...) : E-cadherin transfection increased phosphorylated Akt expression concomitantly with the increase in SCCA2 expression, and the increased SCCA2 expression was inhibited by a PI3K inhibitor
Yamamori et al., Biochem Biophys Res Commun 2004 : These results suggest that PI3K regulates the phosphorylation of NADPH oxidase component p47(phox) by controlling diacylglycerol dependent PKCs but not Akt
McMullen et al., Proc Natl Acad Sci U S A 2007 (Cardiomyopathy, Dilated...) : PI3K ( p110alpha ) signaling negatively regulated G protein coupled receptor stimulated extracellular responsive kinase and Akt ( via PI3K, p110gamma ) activation in isolated cardiomyocytes
Takayama et al., Int Immunol 2013 (MAP Kinase Signaling System) : We also found that the extracellular signal regulated kinase ( ERK ) signaling pathway was activated in a PI3K dependent manner upon FceRI stimulation and that simultaneous inhibition of Akt and ERK resulted in nearly complete blockade of FceRI induced degranulation
Fransson et al., Journal of molecular signaling 2013 : PI3K activity subsequently activates Akt/PKB , and as mutations of PI3K are rare in neuroblastoma and high levels of PI3K subunit p110delta is associated with favorable disease with low p-Akt/PKB, the levels of other PI3K subunits could be important for Akt activation
Yamada et al., Biochem J 2004 : The PI3K inhibitor LY294002 inhibited the ActD induced activation of Akt and p70S6K, and completely abolished the effects of PLD1 or PLD2, whereas inhibition of ERK activity by the MEK inhibitor U0126 had a milder effect
John et al., Dev Biol 2008 : Oocyte-specific ablation of Pten resulted in PI3K induced Akt activation , Foxo3 hyperphosphorylation, and Foxo3 nuclear export, thereby triggering primordial follicle activation, defining the steps by which the PI3K pathway and Foxo3 control this process
Takahashi et al., Am J Physiol 1999 : These results indicate that ANG II stimulates Akt/PKB activity via AT1 receptors in VSMC and that the activities of tyrosine kinase and PI3K are required for this activation
Jang et al., Cell Signal 2005 : Interestingly, there was PI3K dependent activation of AKT , p70S6K, JNKs, and NF-kappaB in response to catalase
Holmström et al., Exp Cell Res 2008 (MAP Kinase Signaling System) : Both EGF and PDGF induced PI3K dependent Akt activation that was not involved in Erk1/2 activation
Kato et al., Biochem Biophys Res Commun 2008 : OML induced ERK phosphorylation was inhibited by specific inhibitors of PI3K and SFKs, and OML induced Akt phosphorylation was inhibited by a inhibitor of SFKs
Steinle et al., Auton Neurosci 2003 : NGF increased choroidal endothelial cell migration by 50 % over control and this was inhibited by pretreatment with LY294002 ( PI3K inhibitor ), Akt inhibitor, and MMP2/9 inhibitor
Miller et al., Breast Cancer Res 2011 (Breast Neoplasms...) : PI3K activates AKT , serum/glucocorticoid regulated kinase ( SGK ), phosphoinositide dependent kinase 1 ( PDK1 ), mammalian target of rapamycin (mTOR), and several other molecules involved in cell cycle progression and survival
Kang et al., Int J Mol Med 2008 (Cell Transformation, Neoplastic) : ERK and PI3K/AKT inhibitors inhibit ECM induced ERK, AKT activation and cell proliferation
Terada et al., Kidney Int 2001 (Dehydration) : PI3-K inhibitors and the dominant negative mutant of PI3-K inhibited the hyperosmolality induced phosphorylation of Akt
Tung et al., J Cell Physiol 2010 (MAP Kinase Signaling System) : Inhibition of PI3K by Wortmannin attenuated EV71 induced Akt and p42/p44 MAPK phosphorylation, but had no effect on PDGFR phosphorylation, suggesting that PDGFR is an upstream and p42/p44 MAPK is a downstream component of PI3K/Akt in these responses
Wang et al., Acta Pharmacol Sin 2013 : The growth of prostate cancer PC-3 cells and B cell type leukemia Raji cells was determined using SRB assay and CCK-8 assay, respectively.Results : The phosphorylation of Akt in Rh30-Myr-p110a, ß, ?, d cells was preferentially inhibited by PI3K isoform-selective inhibitors A66 ( PI3Ka ), TGX221 ( PI3Kß ), AS604850 ( PI3K? ) and CAL-101 ( PI3Kd ), respectively
Campbell et al., Circ Res 2004 (MAP Kinase Signaling System) : ERK1/2 phosphorylation was reduced not only by MAPK pathway inhibitors but also by PI3K and mTOR inhibitors ; when PI3K was inhibited, ERK phosphorylation could be induced by microinjected activated Akt , indicating important cross-talk between the PI3K and ERK1/2 pathways
Kaul et al., Cell Signal 2007 (Glioblastoma) : Introduction of normal PTEN together with H-Ras ( G12V ) into U251 glioblastoma cells reduced the PI3K dependent activation of Akt , but had no effect on vacuolation
Ryu et al., Biocell 2010 (Carcinoma, Squamous Cell...) : Blocking the activation of the PI3K/Akt pathway using LY294002 abolished Akt activation in response to cobalt chloride, suggesting that Akt phosphorylation by cobalt chloride is dependent on PI3K
Viard et al., Nat Neurosci 2004 : We show that the effect of PI3K is mediated by Akt/PKB and specifically requires Ca(v)beta ( 2 ) subunits
Larizza et al., Leukemia & lymphoma 2005 (Acute Disease...) : PI3K dependent activation of AKT and STAT activation was observed in Kasumi-1 cells
Kim et al., Biol Pharm Bull 2007 : Inhibition of PI3K activity by wortmannin completely inhibited KRGE induced angiogenesis and phosphorylation of Akt , ERK1/2, and eNOS, indicating that PI3K/Akt activation is an upstream event of the KRGE mediated angiogenic pathway
Owada et al., PloS one 2013 : We have reported glucose deprivation rapidly induces AKT phosphorylation through PI3K activation
Mendez et al., Mol Cell Biol 1997 : The fact that PKC zeta stimulates general protein synthesis but not activation of p70S6K indicates that PKC zeta activation does not involve the proto-oncogene Akt , which is also activated by PI3K
Sanderson et al., Neurol Res 2009 (Brain Ischemia...) : Insulin induced Akt phosphorylation was suppressed by the PI3K inhibitor wortmannin ... Insulin induces robust PI3K dependent phosphorylation of Akt by 30 minute reperfusion and results in improvement of hippocampal structure and function
Kristof et al., J Pharmacol Exp Ther 2005 (Prostatic Neoplasms) : In human lung epithelial adenocarcinoma ( A549 ) cells, LY303511, like rapamycin, inhibited mTOR dependent phosphorylation of S6K, but not PI3K dependent phosphorylation of Akt
Chien et al., J Lipid Res 2003 : Phosphorylation of Akt stimulated by OxLDL and epidermal growth factor (EGF) was attenuated by inhibitors of PI3-K ( wortmannin and LY294002 ) and intracellular Ca2+ chelator ( BAPTA/AM ) plus EDTA
Biswas et al., J Biol Chem 2013 : Only p110ß was necessary for S1P iduced Akt activation, but both PI3K-C2a and p110ß were required for Rac1 activation
Zhang et al., Planta Med 2007 (Osteoporosis) : Furthermore, puerarin stimulated osteoblastic growth, Akt activation and redistribution were significantly blocked by the specific PI3K inhibitor, LY294002 ... These results strongly suggested that puerarin stimulated osteoblastic proliferation and Akt activation in a PI3K dependent manner
Yu et al., Mol Biol Rep 2010 : However, PI3K inhibitor reduces the increase of phosphorylated Akt level induced by HGF
Rubio et al., J Mol Cell Cardiol 2009 (Myocardial Infarction) : In comparison, overexpression of nuclear targeted Akt does not mediate increased translocation of either PI3K or PDK1 indicating that accumulation of Akt does not drive PI3K or PDK1 into the nuclear compartment
Méndez-Samperio et al., Peptides 2008 : Moreover, there was increased activation of c-Jun N-terminal kinase (JNK) and phosphatidylinositol-3-kinase (PI3K)/Akt in A549 cells infected with M. bovis BCG, and this JNK and PI3K activation was mediated through PKC
Lee et al., Biochem Biophys Res Commun 2004 : TGFbeta mediated phosphorylation of Akt at Ser-473 was inhibited by dominant negative ILK and PI3K inhibitors, LY294002 and wortmannin
Li et al., J Biol Chem 2011 (Thrombosis) : Because of recent reports that arrestins can serve as scaffolds to recruit phosphatidylinositol-3 kinases (PI3K)s to GPCRs, we sought to determine whether arrestins regulate PI3K dependent Akt signaling in platelets, with consequences for thrombosis
Felekkis et al., Mol Cancer Res 2005 (Breast Neoplasms) : Inhibition of PI3K with LY294002 or a dominant negative p85 construct blocked AND-34 mediated Rac and Akt activation
Clark et al., Mol Cancer Ther 2002 (Breast Neoplasms) : Akt promoted breast cancer cell survival because a PI3K inhibitor, LY294002, or transient transfection of a dominant negative Akt mutant inhibited Akt activity and increased apoptosis
Paradis et al., Genes Dev 1998 : This demonstrates that Akt/PKB activity is not necessarily dependent on AGE-1 PI3K activity
Pisitkun et al., American journal of physiology. Renal physiology 2008 (MAP Kinase Signaling System) : Akt activation was blocked by an inhibitor of PI3K , LY294002
Tybulewicz , Eur J Immunol 2004 (Second Messenger Systems) : Unexpectedly, they show that while the BCR induced phosphorylation of the PI3K dependent kinase Akt is reduced in p85alpha-deficient cells, the phosphorylation of two downstream targets of Akt -- FOXO1 and ribosomal protein S6 -- is largely unaffected
Yun et al., Pharmacol Res 2006 : Taken together, these experiments show that the enhanced phosphorylation of Akt/PKB by OA is dependent on PI3K and suggest that this signaling event may be important for the regulation of OA-induced VSMC proliferation
Yang et al., Eur J Pharmacol 2010 : Plumbagin stimulated ERK1/2 activity was attenuated by the MEK1/2 inhibitor PD98059 and Ras inhibitor manumycin A, whereas plumbagin stimulated Akt activity was blocked by the PI3K inhibitor LY294002 ... These results suggest that plumbagin activates NAD ( P ) H oxidase, Src, and PI3K, and that the activated PI3K or PDK1 subsequently stimulate Akt and Ras-Raf-MEK1/2-ERK1/2 in 3T3-L1 cells
Jiang et al., J Hepatol 2009 : PI3K dependent phosphorylation of Akt depended on NADPH oxidase activity and superoxide production
Banfić et al., J Biol Chem 1998 : Both this novel pathway and the activation of PKB/Akt are inhibited by the PI3K inhibitor, wortmannin, and the calpain inhibitor, calpeptin, constituting the first evidence that PtdIns ( 3,4 ) P2 can stimulate PKB/Akt in vivo in the absence of PtdIns ( 3,4,5 ) P3
Strassheim et al., J Immunol 2005 : SHIP ( -/- ) neutrophils demonstrated significantly increased activation of the PI3K dependent kinase Akt after exposure to PGN
Huang et al., J Mol Neurosci 2013 (MAP Kinase Signaling System) : Besides, expression of phosphorylated-AKT and phosphorylated-ERK1/2 in fluoxetine treated NSCs was effectively blocked ( P < 0.05 ) by both PI3-K inhibitor ( LY294002 ) and MEK inhibitor ( PD98059 )
Slouzkey et al., Biol Psychiatry 2013 : To that end, we ( 1 ) monitored AKT phosphorylation in the IC following CTA acquisition and extinction and ( 2 ) inhibited PI3K by local microinjection of the PI3K inhibitor LY294002 at different stages of CTA acquisition and extinction
Mallon et al., Mol Cancer Ther 2010 : We are testing whether dual PI3K/mTOR inhibitors can durably suppress p-Akt , induce cleaved PARP, and cause tumor regression in a diverse set of human tumor xenograft models
Venieratos et al., Cell Signal 2010 : Inhibition of SOCS-1 expression by SOCS-1-specific small interfering RNA restored IRS-2/PI3K mediated Akt phosphorylation suppressed by high glucose
Condorelli et al., Proc Natl Acad Sci U S A 2002 (Cardiomyopathy, Hypertrophic) : In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K dependent Akt activation
Street et al., J Biol Chem 2004 (Carcinoma, Hepatocellular...) : NS5A mediated activation of PI3K resulted in increased phosphorylation and activity of Akt/protein kinase B and concomitantly provided protection against the induction of apoptosis in both replicon harboring cells and cells stably expressing NS5A alone
Qi et al., J Biol Chem 2006 (Carcinoma, Hepatocellular) : The PI3K inhibitor, LY294002, blocked IL-3 stimulated Akt activity and partially blocked Bim ( EL ) phosphorylation
Lee et al., Gastroenterology 2010 (Colitis...) : PI3K inhibition in interleukin-10 ( -/- ) mice impaired colitis induced epithelial Akt and beta-catenin activation, reduced progenitor cell expansion, and prevented dysplasia
Hale et al., Biochem Soc Trans 2007 (Influenza, Human) : Activation of PI3K in virus infected cells is mediated by the viral NS1 protein, which binds directly to the p85beta regulatory subunit of PI3K and causes the PI3K dependent phosphorylation of Akt ( protein kinase B )
Murphy et al., J Biol Chem 2002 : In contrast, like Ras, expression of activated TC21 resulted in membrane translocation and an increase in the PI3K dependent phosphorylation of Akt , and inhibition of PI3K activity interfered with TC21 focus formation
Fischer et al., Lung Cancer 2012 (Mesothelioma...) : The PI3K/mTOR inhibitor NVP-BEZ235 and PI3K inhibitor wortmannin reduced the phosphorylation of downstream target AKT , S6 and 4EBP1 and decreased the SP fraction
Kasukabe et al., Int J Oncol 2013 : The PI3K inhibitor LY294002 also suppressed rapamycin induced phosphorylation of Akt and combined treatment showed synergistic growth inhibition of MCF-7 cells
Cui et al., Mol Cell Biochem 2011 : The aim of this study is to determine whether depletion of PI3K-C2a affects ERK or PKB/Akt activity following stimulation with serum and insulin growth factors in Chinese hamster ovary cells expressing human insulin receptors ( CHO-IR ) and human HepG2 liver cells
Guo et al., J Steroid Biochem Mol Biol 2006 (Endometrial Neoplasms) : PI3K inhibitor, LY294002, stopped the activating Akt in a dose dependent manner and 50 microM LY294002 completely blocked the activation of Akt induced by E2
Miki et al., Basic Res Cardiol 2007 (MAP Kinase Signaling System...) : EPO induced PI3K dependent phosphorylation of Akt in Sham but not in post-MI. EPO increased phosphorylation levels of ERK1/2 both in Sham and post-MI, but this phosphorylation was diminished by a PI3K inhibitor in Sham but not in post-MI
Shin et al., J Gen Virol 2007 : The PI3K-specific inhibitor LY294002 could suppress Akt phosphorylation, suggesting that influenza A virus induced Akt phosphorylation is PI3K dependent
Zhang et al., J Immunol 2007 : Small interfering RNA mediated knockdown of SHIP1 expression increased PI3K dependent Akt activation and subsequently decreased inflammatory cytokine expression, suggesting GC-mediated up-regulation of SHIP1 expression is responsible for the augmentation in inflammatory cytokine production following LPS stimulation
Pfeil et al., Prostate 2004 (Prostatic Neoplasms) : IGF-1, EGF, and heregulin but not PDGF or activators of protein kinase A induced phosphorylation of Akt in DU145 cells and activation was completely blocked by the PI3K inhibitor LY294002
Jiang et al., Adv Cancer Res 2009 (Neoplasms...) : PI3K signaling regulates tumor growth and angiogenesis by activating AKT and other targets, and by inducing HIF-1 and VEGF expression
Amin et al., Int J Oncol 2003 : Similarly, inhibition of PI3K activation by its specific inhibitor LY294002 suppressed Akt phosphorylation
Cao et al., J Mol Endocrinol 2013 : 6Cl-TGQ induced Akt phosphorylation was completely blocked by IR and PI3K inhibitors, while the induced glucose uptake was blocked by the same compounds and a Glut4 inhibitor
Veillette et al., Biol Reprod 2013 : PI3-K inhibition in vivo blocked Akt phosphorylation, reduced Smad2 phosphorylation, and reduced both TGF-beta2 and XIAP expression
Suh et al., J Biol Chem 2003 : These findings suggest an interaction between TSHR and PI3K , which is stimulated by TSH and cAMP and might involve the downstream S6K1 but not Akt/protein kinase B
Zenzmaier et al., Prostate 2013 (Prostatic Hyperplasia...) : DKK3 knockdown did not affect subcellular localization or levels of ß-catenin but attenuated AKT phosphorylation in PrSCs. Consistently the PI3K/AKT inhibitor LY294002 mimicked the effects of DKK3 knockdown
Shineman et al., Biochemistry 2009 : Since the insulin/IGF-1 signaling pathway is tightly regulated by feedback inhibition pathways, we hypothesized that myr-Akt overexpression may be inducing feedback inhibition of PI3K , resulting in impaired APP trafficking
Komori , Clinical calcium 2006 : Phosphoinositide 3-kinase (PI3K)-Akt signaling enhances DNA binding of Runx2 and Runx2 dependent transcription, and Runx2 upregulates PI3K subunits ( p85 and p110 beta ) and Akt
Yu et al., PloS one 2012 (Disease Models, Animal...) : Pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented activation of spinal AKT induced by ephrinB1-Fc. Inhibition of spinal PI3K signaling dose-dependently prevented and reversed pain behaviors and spinal c-Fos protein expression induced by intrathecal injection of ephrinB1-Fc. Inhibition of EphBs receptors by intrathecal injection of EphB1-Fc reduced formalin induced inflammation and chronic constrictive injury induced neuropathic pain behaviors accompanied by decreased expression of spinal PI3K, p-AKT and c-Fos protein
Mehrhof et al., Circulation 2001 : IGF-I-stimulation was followed by a PI3K dependent phosphorylation of AKT and BAD and an MEK1 dependent phosphorylation of extracellular signal regulated kinase ( ERK ) 1 and ERK2
Zhang et al., Biochim Biophys Acta 2011 : Akt phosphorylation was inhibited by the PI3K inhibitor LY294002 ( 10µM ), farnyltranferase inhibitor FTI-276, or transfection with a dominant negative Akt
Miyashita et al., FEBS Lett 2003 : The findings suggest that AM plays significant roles in vascular regeneration, associated with PKA- and PI3K dependent activation of Akt in endothelial cells, and possesses therapeutic potential for vascular injury and tissue ischemia
Suzuki et al., Biochem Biophys Res Commun 2000 (Breast Neoplasms) : While the IGF-I induced activation of PKB/Akt was inhibited by PI3-K inhibitor LY294002 but not by MEK inhibitor PD98059, the activation of both MEK and ERK by IGF-I was inhibited by both
Song et al., Gut 2007 (Adenocarcinoma...) : Dominant negative ( DN ) AKT and LY294002 ( PI3K inhibitor ) or U0126 ( MEK-1/2 inhibitor ) blocked chenodeoxycholic acid ( CD ) and deoxycholic acid ( DC ) mediated COX-2 induction
Thomas et al., J Biol Chem 2002 : Finally, both PI 3-K inhibition by LY294002 and AKT inhibition by transfection of a dominant negative enzyme blocked RSV induced NF-kappaB transcriptional activity
Wlodarski et al., Cancer Res 2005 (Burkitt Lymphoma...) : Both direct Akt ( Akt inhibitors I-III ) and a PI3K inhibitor ( wortmannin at 1 nmol/L ) suppressed Akt phosphorylation without significantly affecting mTOR activation
Renner et al., Carcinogenesis 2007 (Adenocarcinoma...) : Additionally, we describe that the phosphorylation of AKT and eIF4G, as well as the elevation of the Mst1 and RanBP2 protein levels, can be inhibited in vivo in transgenic animals by the PI3K inhibitor LY294002
Blalock et al., J Cell Physiol 2009 (Leukemia) : Increased phosphorylation of AKT and GSK-3alpha was not dependent on PI3K activity ... PKR inhibition augmented levels of p-S473 AKT and p-S21/9 GSK-3alpha/beta in the presence of the PI3K inhibitor, LY294002, but was unable to augment GSK-3alpha or beta phosphorylation in the presence of the AKT inhibitor, A443654
Banerjee et al., Breast Cancer Res Treat 2012 (Breast Neoplasms...) : Pg extract also induced SHIP-1 expression and this was accompanied by downregulation of miRNA-155 and inhibition of PI3K dependent phosphorylation of AKT
Chuenkova et al., Proc Natl Acad Sci U S A 2001 (Chagas Disease) : In contrast, the Cys-rich domain of TS did not block apoptosis in Schwann cells overexpressing dominant negative Akt or constitutively active PTEN, a negative regulator of PI3K/Akt signaling
Marcinkowska et al., Anticancer Res 2003 : Phosphatidylinositol-3 kinase dependent activation of Akt does not correlate with either high mitogenicity or cell migration induced by FGF-1
Kondo et al., Oncol Rep 2005 : We found that both PI 3-K inhibitors, wortmannin and LY294002, markedly suppressed phosphorylation of Akt and Bad in HL-60 cells
Uddin et al., Blood 2006 (Lymphoma, B-Cell...) : AKT was phosphorylated in 5 of 5 DLBCL cell lines and inhibition of PI3K caused dephosphorylation/inactivation of constitutively active AKT, FOXO transcription factor, and GSK3 in LY-sensitive cell lines
Camacho-Leal et al., J Cell Physiol 2007 (MAP Kinase Signaling System) : Conversely, anti-alpha5 antibody inhibited the PI3-K mediated activation of Akt , implying the involvement of outside-in and inside-out signaling in integrin activation
Omori et al., Immunity 2006 : PI3K dependent activation of the serine-threonine kinase, Akt , suppressed CSR, in part, through the inactivation of the Forkhead Box family ( Foxo ) of transcription factors
Fresno Vara et al., Mol Biol Cell 2001 : In contrast, they inhibited the PRL dependent stimulation of the SFKs substrate Sam68, the phosphorylation of the tyrosine phosphatase Shp2, and the PI3K dependent Akt and p70S6k serine kinases
Qiu et al., Mol Hum Reprod 2004 : In the presence of PI3K inhibitors ( Wortmannin ), EGF stimulated trophoblast migration and phosphorylation of AKT and P70S6K ( Thr ( 389 ) and Thr ( 421 ) /Ser ( 424 ) ) were decreased, while EGF induced ERK phosphorylation was not affected
Sugimori et al., J Bone Miner Metab 2005 : Akt was rapidly phosphorylated in response to BMP-2 treatment ; however, the inhibition of PI3K by Wortmannin markedly reduced the phosphorylation of Akt by BMP-2
Huber et al., Mol Cell Biol 2003 : We demonstrate that both nephrin and CD2AP interact with the p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K) in vivo, recruit PI3K to the plasma membrane, and, together with podocin, stimulate PI3K dependent AKT signaling in podocytes
Delcommenne et al., Proc Natl Acad Sci U S A 1998 : ILK is thus a receptor-proximal effector for the Pi(3)K dependent , extracellular matrix and growth factor mediated, activation of PKB/AKT , and inhibition of GSK-3
Zhang et al., Biochem Pharmacol 2007 (Prostatic Neoplasms) : In PC-3 cells, CMEP has been found to inhibit only AKT activation at both normal and serum-starvation conditions, not to inhibit PI3K , PDK1, or MAPK
De Gregorio et al., Oncogene 2007 : Similarly, binding of PI3K to p21Ras and activation of AKT , a downstream PI3K target, were severely impaired in cells expressing the p85A mutant
Velling et al., EMBO Rep 2004 : Here we show that PI3K dependent phosphorylation of Akt in response to ligation of beta1-integrins occurs efficiently in the absence of FAK tyrosine phosphorylation
Gagnon et al., Gynecol Oncol 2004 (Uterine Neoplasms) : KLE cells remained resistant to PI 3-K inhibitor, indicating that Akt phosphorylation might be, in part, independent of PI 3-K in this cell line
Merighi et al., J Biol Chem 2005 (MAP Kinase Signaling System...) : Here, we show that the A ( 3 ) adenosine receptor agonist Cl-IB-MECA stimulates PI3K dependent phosphorylation of Akt leading to the reduction of basal levels of ERK1/2 phosphorylation, which in turn inhibits cell proliferation ... Using A375 cells, we show that A ( 3 ) adenosine receptor stimulation results in PI3K dependent phosphorylation of Akt , leading to the reduction of basal levels of ERK1/2 phosphorylation, which in turn inhibits cell proliferation
Buitrago et al., J Cell Biochem 2012 : Of relevance, Src and PI3K are involved in Akt activation and in MHC and myogenin increased expression by 1a,25 ( OH ) ( 2 ) D ( 3 )
Miggin et al., Mol Pharmacol 2002 : Additionally, PKB/Akt was activated through TPalpha and TPbeta in a PI3K dependent manner
Gingery et al., J Cell Biochem 2003 (MAP Kinase Signaling System) : PI3K inhibition also blocked MEK1/2, ERK1/2, and AKT phosphorylation and NFkappaB activation in purified osteoclasts
Tawa et al., Circ Res 2010 (Disease Models, Animal...) : Rap1 regulated the interaction between afadin and phosphatidylinositol 3-kinase (PI3K), recruitment of the afadin-PI3K complex to the leading edge, and the activation of Akt , indicating the involvement of Rap1 and afadin in the PI3K-Akt signaling pathway
Rosner et al., Am J Pathol 2006 (Atherosclerosis) : IFN-gamma also stimulated Akt activity, and both Fas trafficking and Stat1 activation were inhibited by blocking PI3K , Akt, or Jak-2
Barata et al., J Exp Med 2004 (Precursor Cell Lymphoblastic Leukemia-Lymphoma) : IL-7 induced PI3K dependent phosphorylation of Akt and its downstream targets GSK-3, FOXO1, and FOXO3a
Kamo et al., Hepatology 2013 (Liver Diseases...) : A specific PI3K blockade inhibited Akt/ß-catenin signaling, increased Foxo1 mediated TLR4-driven local inflammation, and recreated cardinal features of liver IR injury
Haeussler et al., J Biol Chem 2013 : Knockdown of H-Ras blocked VEGF induced PI3K dependent Akt ( Ser-473 ) and eNOS ( Ser-1177 ) phosphorylation and nitric oxide dependent cell migration, demonstrating the essential role of H-Ras
Zhang et al., J Cell Physiol 2012 (Carcinoma, Non-Small-Cell Lung...) : EGF stimulated IL-8 production, phosphorylation of Akt and Erk, and cell proliferation and movement could be inhibited by EGFR inhibitor ( Erlotinib ), PI3K inhibitor ( GDC-0941 BEZ-235 and SHBM1009 ), and ERK1/2 inhibitor ( PD98059 )
Yu-Shengyou et al., BioMed research international 2013 : The PI3K inhibitor LY294002 blocked p-Akt and p-GSK3 ß expressions in podocytes
Dong et al., Cancer Res 2001 (Carcinoma, Squamous Cell...) : Inhibitors of MEK ( U0126 ) and PI3K ( LY294002 ) blocked p42/p44 ( erk ) and Akt , respectively, and partially blocked HGF induced production of IL-8 and VEGF, whereas the combination of U0126 and LY294002 completely inhibited expression of IL-8 and VEGF by UMSCC-11A
Hatano et al., Am J Physiol Gastrointest Liver Physiol 2001 : The PI3K inhibitor LY-294002 blocks TNF-alpha- and Fas mediated Akt phosphorylation
Ruiter et al., Anticancer Drugs 2003 (Neoplasms, Glandular and Epithelial) : We found that growth factor induced Akt/PKB activation in these cells is dependent on PI3K and that all three ALPs inhibited this pathway in a dose dependent manner
Stoica et al., Mol Endocrinol 2003 (Breast Neoplasms) : Treatment of cells with estradiol resulted in phosphorylation of Akt and a 9-fold increase in Akt activity in 10 min. Akt activation was blocked by wortmannin and LY 294,002, two inhibitors of PI 3-K ; by genistein, a protein tyrosine kinase inhibitor and an ER agonist ; by AG825, a selective ErbB2 inhibitor ; and by the antiestrogens ICI 182,780 and 4-hydroxy-tamoxifen ; but not by rapamycin, an inhibitor of the ribosomal protein kinase p70S6K ; nor by AG30, a selective epidermal growth factor receptor inhibitor
Mori et al., Virus Genes 2006 (Burkitt Lymphoma) : Akt phosphorylation and cell growth were inhibited by PI3-K specific inhibitor LY294002 in a dose dependent manner
Huang et al., Mol Cell Neurosci 2005 : Insulin also induced rapid and long-term ( 30 h ) PI 3-K dependent phosphorylation of Akt and cAMP response element binding protein ( CREB )
Tian et al., J Dig Dis 2012 (Stomach Neoplasms) : Specific ERK1/2 inhibitor PD98059 and PI3K inhibitor wortmannin reduced phosphorylation of ERK1/2 and Akt , respectively and blocked ghrelin- and des-acyl ghrelin induced AGS cell proliferation
Huang et al., J Cell Biochem 2012 : Inhibition of calcineurin further reduced the phosphorylation of ERK and AKT ( at thr 308 ) and inhibited the activation of Ras, but inhibitors of MAPK or PI3K signaling did not affect the circadian rhythm of calcineurin activity
Nakamura et al., Rheumatol Int 2007 (Sjogren's Syndrome) : Chemical inhibition of PI3K-Akt by LY294002/wortmannin did not affect EGF mediated NF-kappaB p65 nuclear translocation ; and NF-kappaB inhibition by Bay 11-7082 did not suppress Akt phosphorylation
Lee et al., Int Immunopharmacol 2008 : Interestingly, emodin induced the activation of phosphatidylinositol 3-kinase (PI3K), Akt and mitogen activated protein ( MAP ) kinases, but those inductions by emodin were completely inhibited by the PI3K inhibitor, LY294002, suggesting that the up-regulation of BMP-2 by emodin could be mediated through the activation of both Akt and MAP kinases by activating PI3K
Esposito et al., Mol Pharmacol 2008 : However, phosphoinositide dependent kinase-1, Akt/protein kinase B, and protein kinase Czeta activities were rapidly induced after SR141716 treatment of L6 cells in a PI3K dependent manner
Gupta et al., Blood 2009 (Lymphoma, Follicular) : Activation of PI3K via APRIL results in phosphorylation of Akt and mammalian target of rapamycin (mTOR) and the mTOR-specific substrates p70S6 kinase and 4E-binding protein 1 in a TACI dependent manner
Iwase et al., Int J Oncol 2007 (Carcinoma, Squamous Cell...) : We found that two PI 3-K inhibitors, wortmannin and LY294002, markedly suppressed the phosphorylation of Akt in OSCC cells
Zhao et al., J Lipid Res 2012 : Further studies showed that TNF-a decreased expression of the antiapoptotic proteins Bcl-2 and Bcl-xL, decreased I?Ba and PPAR?, and also inhibited PI3K dependent Akt and EGFR signaling
Rajala et al., Biochemistry 2004 : These results suggest that multiple signaling pathways could regulate the PI3K activity and subsequent activation of Akt in the retina
Kiaer et al., Endocrine 2009 : In conclusion, it is suggested that albumin may be a survival factor for pancreatic beta cells through scavenging of reactive oxygen species and by PI3K dependent activation of Akt
Hashikawa-Hobara et al., Diabetes 2012 (Insulin Resistance) : These results suggest that the decrease of AT(2)R mediated neurite outgrowth in FDRs is likely to be the result of decreased PI3K dependent Akt activation
Rajala et al., J Virol 2005 : The results presented in this paper provide the first direct evidence that PI3K mediated Akt activation in adenovirus infected corneal cells may contribute to viral pathogenesis by the prolongation of cell viability
Morisco et al., Circ Res 2005 (Insulin Resistance) : Short-term stimulation induces an additive effect on insulin induced glucose uptake, and this effect is mediated by phosphorylation of Akt in threonine 308 through PKA/Ca2+ dependent and PI3K independent pathway, whereas insulin evoked threonine phosphorylation of Akt is exclusively PI3K dependent
Hanson et al., Mol Cell Endocrinol 2010 : The ERK pathway inhibitor, U0126, retarded SS-14 stimulated phosphorylation of ERK 1/2, whereas the PI3K inhibitor, LY294002, blocked SS-14 stimulated phosphorylation of Akt
Zhang et al., J Immunol 2007 (Body Weight) : Inflammatory cytokine overexpression by 11betaHSD1 ( -/- ) splnMphi results from an increased activation of NF-kappaB- and MAPK signaling cascades and an attenuated PI3K dependent Akt activation
Kondo et al., Oral Oncol 2006 (Carcinoma, Squamous Cell...) : We found that both PI 3-K inhibitors, wortmannin and LY294002, markedly suppressed the phosphorylation of Akt and accelerated Fas mediated apoptosis in OSCC cells
Kim et al., J Biol Chem 2009 : In addition, GPVI induced Akt phosphorylation in the presence of ADP antagonists was completely inhibited by PI3K inhibitor LY294002 and PI3Kbeta inhibitor TGX-221 indicating an essential role of PI3Kbeta in Akt activation directly downstream of GPVI
Shi et al., Mol Cancer Ther 2005 (Multiple Myeloma) : Rapamycin enhanced basal AKT activity, AKT phosphorylation, and PI3K activity in multiple myeloma cells and prolonged activation of AKT induced by exogenous IGF-I
Lahair et al., Antioxid Redox Signal 2006 : In contrast, hydrogen peroxide induced phosphorylation of Akt on serine 473 ( S473 ) was downregulated by both PI3K and CaM-K inhibition, indicating that hydrogen peroxideinduced phosphorylation of Akt on S473 was largely dependent on both PI3K and a CaM-K activity
Liu et al., J Cell Biochem 2009 : A specific PI3K inhibitor, wortmannin, blocked Akt phosphorylation and abrogated the beneficial effect of DMOG
Samarin et al., Journal of cell communication and signaling 2009 : In endothelial cells activation of PI3K - AKT signaling was inversely related to CCN2 expression
Nagoshi et al., J Clin Invest 2005 (Myocardial Reperfusion Injury) : Biochemical analyses demonstrated that chronic Akt activation induces feedback inhibition of PI3K activity through both proteasome dependent degradation of insulin receptor substrate-1 (IRS-1) and inhibition of transcription of IRS-1 as well as that of IRS-2
Muñoz-Alonso et al., J Pharmacol Exp Ther 2008 (Melanoma) : By using inhibitors, we found that JNK and p38 MAPK activation depends on Rac1 but not on phosphatidylinositol 3-kinase (PI3K), whereas AKT activation is independent of Rac1 but requires PI3K activity
Knobbe et al., Brain Pathol 2003 (Brain Neoplasms...) : In contrast, we did not find any aberrations in the inositol polyphosphate phosphatase like-1 gene ( INPPL1 ), whose gene product may also counteract Pi3k dependent Akt activation
Haga et al., J Vasc Surg 2003 (Disease Models, Animal...) : Both PI3K inhibitors specifically inhibited the increase in Akt phosphorylation in SMC exposed to oscillatory SS
Díaz-Montero et al., Eur J Cancer 2006 (Osteosarcoma) : The activity of Akt was found to be upregulated in anoikis resistant SAOSar cells and the pharmacological inhibition of PI3-K activity restored sensitivity to anoikis resistant cells, reconfirming the critical role of PI3-K/Akt pathway in cell survival
May et al., J Biol Chem 2010 : Phosphatidylinositol 3-kinase gamma-selective inhibitors blocked PACAP stimulated Akt phosphorylation in primary neuronal cultures and in PAC(1)HOP1 overexpressing cell lines ; RNA interference mediated knockdown of the receptor effectors attenuated PACAP mediated Akt activation
Lin et al., Toxicon 2010 (Breast Neoplasms) : Moreover, the PI3K inhibitor wortmannin blocked activation of STAT3 and Akt without affecting the JAK2 activation, whereas JAK2 inhibitor AG490 suppressed the levels of phospho-STAT3, phospho-Akt, and PI3K, suggesting that PI3K activation occurs after JAK2 phosphorylation, and both PI3K and JAK2 kinases cooperate to mediate STAT3 and Akt phosphorylation
She et al., Clin Cancer Res 2003 (Breast Neoplasms) : We show here that pharmacologic down-regulation of constitutive PI3K/Akt pathway signaling using the PI3K inhibitor LY294002 similarly restores EGFR stimulated Akt signaling and sensitizes MDA-468 cells to ZD1839
Zhang et al., Brain Res Mol Brain Res 2002 : The effects of DHEA on neural cell survival and activation of Akt were not blocked by the steroid hormone antagonists flutamide and tamoxifen, but both were blocked by a PI3-K inhibitor, LY294002
Maffucci et al., PloS one 2009 : Finally we show that PI3K dependent PLCgamma1 activation regulates FGF-2 mediated phosphorylation of Akt at its residue Ser473, determined by Western blotting analysis ... Furthermore these data unveil a novel role for PLCgamma1 as a mediator of PI3K dependent Akt activation and as a novel key regulator of different Akt dependent processes
Forti et al., Biochemistry 2002 (Adrenal Cortex Neoplasms) : Inhibitors of PI3K lead to rapid dephosphorylation of Akt/PKB and block phosphorylation of Akt/PKB promoted by FGF2
Harvey et al., Arterioscler Thromb Vasc Biol 2007 (Atherosclerosis) : AKT was the downstream target for PI3K action
Baki et al., J Neurosci 2008 (Alzheimer Disease...) : Expression of exogenous WT PS1 or constitutively active Akt in PS1-/- neurons stimulates PI3K signaling and suppresses both caspase-3 activity and dendrite retraction
Akiyama et al., FEBS J 2006 : The PI3K inhibitor, LY294002, blocked cartducin stimulated Akt phosphorylation and a decrease in cartducin induced DNA synthesis in N1511 cells was also observed
Reséndiz et al., Journal of thrombosis and haemostasis : JTH 2007 : Akt phosphorylation approximately 60 s after PAR1 stimulation became entirely dependent on the purinergic receptor P2Y(12) and the activation of PI3K
Shortt et al., Blood 2013 (Lymphoma, B-Cell) : Moreover, apoptosis was initiated at drug concentrations insufficient to antagonize PI3K/mTORC2 regulated AKT phosphorylation
Bhaskar et al., Molecular neurodegeneration 2009 : Finally, our results also demonstrate that Abeta oligomer treated neurons exhibit elevated levels of activated Akt and mTOR ( mammalian Target Of Rapamycin ) and that PI3K , Akt or mTOR inhibitors blocked Abeta oligomer induced neuronal CCEs
Okano et al., J Biol Chem 2000 (Esophageal Neoplasms) : PI3K inhibitors, wortmannin or LY294002, significantly blocked the Akt kinase activity induced by EGF
Maeda et al., Biochem Biophys Res Commun 2004 : Expression of Gab1 PI3K-m in SK-N-MC human primitive neuroectodermal tumor cells expressing wild-type RET markedly impaired Akt phosphorylation, Rac1 activation, and lamellipodia formation that were induced by GDNF whereas expression of Gab1 SHP2-m partially impaired Erk activation
Dackour et al., In Vitro Cell Dev Biol Anim 2005 (Laryngeal Neoplasms...) : Using ribonucleic acid interference to reduce protein levels of integrin linked kinase 1 or phosphoinositide dependent protein kinase 1, intermediates in the activation of Akt by PI3K , or reducing levels of Akt-1 itself did not inhibit K13 expression by normal laryngeal keratinocytes
Margolis et al., J Physiol 2011 : Using a variety of blockers we determined that the augmentation is probably due to insertion of GABA ( A ) Rs into the synapse by a mechanism that is G-protein independent and mediated by activation of Akt via PI3K
Kelley et al., J Biol Chem 1999 : In normal human monocytes, M-CSF increased the levels of tyrosine phosphorylated proteins and induced Akt activation in a PI3K dependent manner
Yamaki et al., Exp Cell Res 2007 : On the other hand, the regulation of anoikis by RhoG required phosphatidylinositol 3-kinase (PI3K) activity, and constitutively active RhoG bound to the PI3K regulatory subunit p85alpha and induced the PI3K dependent phosphorylation of Akt
Zhang et al., Front Biosci (Schol Ed) 2013 : Exposure of cells to EGF activated the AKT phosphorylation, whereas EGFR and PI3K inhibitors blocked EGF induced AKT phosphorylation in a dose dependent manner
Ma et al., Biochem Pharmacol 2004 : Furthermore, DEP promoted phosphorylation of Akt , a substrate of phosphatidylinositol 3-kinase (PI3K), on Ser-473 and Thr-308 in a PI3K dependent manner, and enhanced phosphorylation of down-stream p70/p85 S6 kinases ( p70/p85S6K ) as well as glycogen synthase kinase-3beta ( GSK-3beta )
Kettritz et al., J Am Soc Nephrol 2002 : PI3-K inhibition by LY294002 blocked both Akt phosphorylation and superoxide generation
Berna et al., J Biol Chem 2010 : Akt activation by CCK and gastrin could be inhibited by the PI3K inhibitor wortmannin
Schwab et al., Apoptosis 2005 (Neuroblastoma) : PI3-K inhibitor, LY294002, reduced IGF-I stimulated phosphorylation of FKHR, FKHRL1, and Akt , but did not affect Erk phosphorylation
Zhang et al., PloS one 2011 : In adult C57BL/6 mice, acute ßAR stimulation induced significant increases in PI3K activity and activation of Akt and ERK1/2 in the heart, but not in lungs or livers
Rangaswami et al., J Biol Chem 2012 (Mechanotransduction, Cellular) : Both pathways cooperated to increase PI3K dependent Akt phosphorylation and were necessary for FSS to induce nuclear translocation of ß-catenin, c-fos, and cox-2 gene expression and osteoblast proliferation
de Araújo et al., J Cancer Res Clin Oncol 2010 (Colorectal Neoplasms) : Furthermore, we provided evidence that PI3K inhibition leads to a decrease in p-Akt and p-GSK-3ß and increased p-ß-catenin levels, which in turn controlled cell proliferation, motility, and colony formation
Gallagher et al., Oncogene 2012 (Cell Transformation, Neoplastic...) : We also investigated the effect of targeted PI3K/mTOR inhibition on PI3K/Akt/mTOR and Erk1/2 signaling, and the potential effects on glycemia
Doepfner et al., Leukemia 2007 (Acute Disease...) : Moreover, downregulation of the class Ia PI3K isoforms p110beta and p110delta by RNA interference impaired IGF-I stimulated Akt activation, cell growth and survival in AML cells
Saito et al., Stroke 2004 (Brain Ischemia) : We administered the PI3-K inhibitor, LY294002, into mouse brains after tFCI and examined the role of PI3-K in the ILK pathway and expression of the ILK/Akt complex by immunohistochemistry, Western blot analysis, and coimmunoprecipitation
Mawrin et al., Clin Cancer Res 2005 (Meningeal Neoplasms...) : Atypical and malignant meningiomas showed higher levels of phospho-Akt compared with benign tumors, and their proliferation could be inhibited by PI3K blocking using wortmannin