Gene interactions and pathways from curated databases and text-mining

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EPHB2 — PIK3R1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Mounho et al., Toxicol Appl Pharmacol 1999 : The pathway leading to peroxisome proliferator induced ERK activation is different than that induced by phorbol ester or EGF, since the PI3K inhibitors had no effect on ERK phosphorylation induced by these agents
Li et al., Eur J Immunol 2000 (MAP Kinase Signaling System) : Thus, in normal human B cells, PI3K is upstream of the Ca2+ response while PI3K , Ca2+ release and protein kinase C are all required for ERK2 activation, and CD19 enhances the MAPK cascade at multiple levels, depending on the state of differentiation
York et al., Mol Cell Biol 2000 : Both inhibitors of PI3-K and inhibitors of endocytosis prevent GTP loading of Rap1 and block sustained ERK activation by NGF ... PI3-K and endocytosis may also regulate ERK signaling at a second site downstream of Ras, since both rapid ERK activation and the Ras dependent activation of the MAP kinase kinase kinase B-Raf are blocked by inhibition of either PI3-K or endocytosis
Zubilewicz et al., Invest Ophthalmol Vis Sci 2001 : Inhibition of PI 3-K/p70 ( S6K ) activities also unexpectedly inhibited ERK activity, whereas the converse was not observed, suggesting that PI 3-K acted upstream from ERK and controlled this pathway for CEC proliferation
Chaudhary et al., J Cell Biochem 2001 : Taken together, our data for the first time revealed that the activation of ERK1/2 by PDGF-BB is mediated by PI 3-K , and secondly, Akt is activated by PDGF-BB and EGF but not by FGF-2 in human and mouse osteoblastic cells
Santiago-Pérez et al., J Cell Physiol 2001 (MAP Kinase Signaling System) : Accordingly, ERK1/2 phosphorylation induced by UTP was inhibited by the PI3K inhibitors, wortmannin and LY294002, and the c-src inhibitors, radicicol and PP2, but not by inhibitors of protein kinase C ( PKC )
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
Nosaka et al., Biochem Biophys Res Commun 2001 (Fibrosarcoma) : The PI3K inhibitor LY294002 significantly inhibited TNFalpha activation of Rac as well as Erk and abolished that of the PI3K target Akt, without showing any inhibitory effects on JNK and p38 activation
Guillemot et al., J Biol Chem 2001 (MAP Kinase Signaling System) : Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a p21(ras)/Raf-1/MEK/ERK dependent manner, and also involves PI3K and SHP-2
Mograbi et al., J Biol Chem 2001 : Thus, both PI3K and Akt act in concert to finely regulate the level of ERK
Rojnuckarin et al., J Biol Chem 2001 : PKCzeta and PI3K also contribute to TPO induced ERK activation in MKs, confirming their physiological relevance
Stroppolo et al., J Neurochem 2001 : We also found that inhibition of PI3K reduces BDNF induced Erk phosphorylation, indicating that cross-talk between these pathways may play a prominent role in MSNs
Park et al., J Leukoc Biol 2002 : p43-Dependent activation of ERK was inhibited by PI3-K inhibitors, and the activation of p38 MAPK was not
Yu et al., J Biol Chem 2002 : These experiments demonstrate that EGF and HGF mediated ERK activation result in divergent effects on Gab1/PI3K signaling
Corbetta et al., J Clin Endocrinol Metab 2002 (Adenoma...) : PI3K blockade by wortmannin, known to prevent G protein betagamma subunit effect on ERK1 and -2, induced a 30 % reduction of the Ca ( o ) ( 2+ ) -stimulated ERK1 and -2 activity
Iijima et al., Circulation 2002 : To elucidate the signaling mechanism underlying the RWP effects, we investigated the effects of RWPs on the activity of PI3K and the phosphorylation of MAPK pathways in PDGF-BB stimulated SMCs. RWPs inhibited the PI3K activity and p38 ( MAPK ) phosphorylation, but not ERK1/2 phosphorylation, in a concentration dependent manner
Lindvall et al., Biochem Biophys Res Commun 2002 : In addition, we have investigated the involvement of PI 3-K in the MAPKs and ERK and JNK phosphorylation, in the presence or absence of Btk
Pinzani et al., Frontiers in bioscience : a journal and virtual library 2002 : In addition, PI 3-K is involved in the activation of the Ras-ERK pathway in human HSC, although it is not strictly necessary, since established PI 3-K inhibitors inhibit ERK activation only by 40-50 %
Gentili et al., J Cell Biochem 2002 (MAP Kinase Signaling System) : We report here that PI3K is also required for PTH activation of the mitogen activated protein kinases ERK1 and ERK2
Hetman et al., J Biol Chem 2002 : Here, we report that inhibition of ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and PI3K were required for brain derived neurotrophic factor (BDNF) suppression of GSK3beta activity
Galve-Roperh et al., Mol Pharmacol 2002 (Astrocytoma) : In conclusion, CB(1) induced ERK activation was mediated by PI3K ( IB ) and this effect may have important consequences in the control of cell death/survival decision
Schwindt et al., Biochemistry 2003 (Adrenal Cortex Neoplasms) : PKC inhibitor Go6983 and PI3K inhibitors wortmannin and LY294002 all inhibit ERK1/2 activation by AVP, but not by FGF2
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
Acconcia et al., IUBMB Life 2003 : At the present meagre information is available for the role played by the rapid hormone action mechanism ( s ) ( i.e., activation of ERK , PI(3)K , PKC-alpha ) in modulating E2-induced gene promoter activity
Oh et al., J Biol Chem 2003 : PI3K activation is required for the activation of protein kinase C (PKC)-alpha and p38 kinase and inhibition of ERK1/2
Xu et al., J Biol Chem 2003 (Diabetic Nephropathies) : Surprisingly, inhibition of PI3K blocks both ERK and Ki-Ras activation
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 %
Laprise et al., J Cell Physiol 2004 : Akt, MEK, and ERK activation levels return to control levels 60 min after calcium restoration ; ( 2 ) the use of E-cadherin blocking antibodies efficiently prevents Akt phosphorylation and MEK-ERK inhibition after 70 min of calcium restoration ; ( 3 ) using the PI3K inhibitor LY294002 ( 15 microM ) in calcium switch experiments, we demonstrate that the assembly of adherens junctions activates Akt activity and triggers the inhibition of ERK1/2 activities in a PI3K dependent manner ; ( 4 ) adenoviral infection of confluent Caco-2/15 cells with a constitutively active mutant of Akt1 strongly represses ERK1/2 activities ; ( 5 ) inhibition of PI3K abolishes Akt activity but leads to a rapid and sustained activation of the MEK-ERK1/2 in confluent differentiating Caco-2/15 cells, but not in undifferentiated growing Caco-2/15 cells
Schmidt et al., BMC biology 2004 (MAP Kinase Signaling System) : Surprisingly, three structurally different PI3K inhibitors block Ras, MEK and Erk activation in PEPs by Epo
Elad-Sfadia et al., J Biol Chem 2004 : Thus, unlike galectin-1, which prolongs Ras activation of ERK and inhibits PI3-K , K-Ras-GTP/galectin-3 interactions promote, in addition to PI3-K and Raf-1 activation, a third inhibitory signal that attenuates active ERK
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
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
Kim et al., Cell Signal 2004 : We have characterized the role of Drosophila PI3K and AKT in ERK pathway activation involving insulin induced proliferation using Drosophila Schneider cells
Choi et al., J Recept Signal Transduct Res 2004 : To study the role of PI3K in insulin stimulation of ERK , we employed PI3K inhibitor LY294002 and mouse embryonic R- fibroblasts lacking IGF-1 receptors ... In these R- cells, PI3K inhibition by LY294002 enhanced insulin stimulation of ERK phosphorylation whereas LY294002 inhibited insulin stimulation of Akt phosphorylation ... Increased insulin stimulation of ERK by PI3K inhibition was mediated by the MEK/ERK pathway, but did not involve inhibitory Ser259 phosphorylation of raf that was reported to be mediated by Akt ... In summary, PI3K inhibition in R- cells enhanced insulin stimulation of ERK phosphorylation by mechanisms involving enhancement of IRS-1 tyrosine phosphorylation, IRS-1-Grb2 complex formation and the ras/MEK/ERK pathway
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
Zhuang et al., J Neurosci 2004 (Hyperalgesia...) : ERK activation by capsaicin and NGF was also blocked by PI3K inhibitors ... Therefore, PI3K induces heat hyperalgesia, possibly by regulating TRPV1 activity, in an ERK dependent manner
Gerasimovskaya et al., J Appl Physiol 2005 : However, activation of PI3K was not required for activation of ERK1/2 , implying a parallel involvement of these pathways in the proliferative response of fibroblasts to hypoxia
Duca et al., Mol Pharmacol 2005 : The simultaneous inhibition of PKA and PI3K , by N- ( 2- ( p-bromocinnamylamino ) ethyl ) -5-isoquinolinesulfonamide ( H89 ) and 2- ( 4-morpholynil ) -8-phenyl-4H-1-bemzopyran-4-one ( LY294002 ), respectively, blocked MEK1/2 and ERK1/2 phosphorylation, as did lactose, an EBP antagonist
Shah et al., J Cell Physiol 2006 (MAP Kinase Signaling System) : However, ERK1/2 activation by these agonists in these cells was independent of PI3K activation ... In contrast, agonist stimulation of HEK 293 cells stably expressing AT1-R caused ERK1/2 phosphorylation that was independent of EGF-R transactivation but required PI3K activation
Chen et al., Nat Neurosci 2005 : Inhibitors of PI3K signaling also blocked increases in ERK/MAP kinase activity associated with memory retrieval
Galaria et al., J Surg Res 2005 : ATF induces akt phosphorylation through a PI3K mediated but ras independent mechanism while both ras and PI3K are required for ERK1/2 activation
Wain et al., Cell Signal 2005 : However, co-ligation of the B cell antigen receptor and FcgammaRIIB inhibits the PI3K dependent phosphorylation of PKB and ERK1/2 in response to CXCL12
El-Assal et al., Gastroenterology 2005 (Colitis, Ischemic...) : HB-EGF enhances restitution after intestinal ischemia/reperfusion via PI3K/Akt and MEK/ERK1/2 activation
Slomiany et al., IUBMB Life 2005 : The impedance by leptin of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of PI3K , as well as by ERK inhibitor, PD98059
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
Jung et al., J Clin Immunol 2005 (MAP Kinase Signaling System...) : The inhibition of PI 3-K did not significantly activate p38 MAPK or ERK 1/2 in PPD stimulated human monocytes
Hagiwara et al., Nephrol Dial Transplant 2006 (Diabetes Mellitus, Type 2...) : EPA and specific inhibitors of ERK1/2, JNK and PI3K decreased levels of MCP-1 in MMCs. EPA suppressed phosphorylation of ERK1/2 and p38 in MMCs, and decreased p-ERK positive cells in glomeruli of KKAy/Ta mice
Robertson et al., J Immunol 2005 : We demonstrate that PI3K is required for TCR stimulated ERK activation in CTL, which we have shown previously to be required for CTL degranulation ... These studies demonstrate that PI3K regulates ERK activity leading to CTL degranulation, and identify paxillin as a target of ERK downstream of the TCR
David et al., J Immunol 2005 : In that pharmacological inhibitors of PI3K inhibited LPS induced activation of p21Ras, but not activation of ERK , we concluded that LPS induced activation of ERK occurs through a pathway that is not dependent on the activation of p21Ras
Liu et al., Eur J Cell Biol 2006 : PI3K is required for insulin stimulated but not EGF stimulated ERK1/2 activation ... Here, we report that two structurally distinct PI3K inhibitors, wortmannin and LY294002, inhibited insulin induced activation of ERK1/2 but had no effect on EGF induced activation of ERK1/2 in hepatocellular carcinoma BEL-7402 and SMMC-7721 cells, breast cancer MCF-7 cells, and prostate cancer LNCaP cells ... These results indicate that PI3K plays different roles in the activation of Ras/ERK1/2 signaling by insulin and EGF, and that insulin stimulated, but not EGF stimulated, ERK1/2 and Akt signalings diverge at PI3K
Simó et al., Cereb Cortex 2007 (MAP Kinase Signaling System) : Our findings demonstrate that Reelin triggers ERK signaling in an SFK/mDab1- and PI3K dependent manner and that ERK activation is required for Reelin dependent transcriptional activation and the detachment of neurons migrating from the SVZ
Zanin-Zhorov et al., J Clin Invest 2006 : The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K , and p38, and were further enhanced by inhibition of ERK
Xu et al., Am J Physiol Lung Cell Mol Physiol 2006 (Hyperoxia...) : Taken together, these data demonstrate that mtALDH overexpression attenuates hyperoxia induced cell death in lung epithelial cells through reduction of ROS, activation of ERK/MAPK , and PI3K-Akt cell survival signaling pathways
Saegusa et al., Mol Immunol 2007 : PI3K inhibitors suppressed the activation of extracellular regulated kinase (ERK) , a member of the mitogen activated protein kinases, by CpG-ODN
Mannella et al., J Neurosci 2006 (Alzheimer Disease...) : E2-induced phosphorylation of Akt, was first apparent at 10 min and maximal at 30 min. Simultaneously, E2-induced pERK1/2 was first apparent at 5-10 min and maximal at 30 min. Inhibition of PI3K completely blocked E2 activation of pAkt at 10 and 30 min and blocked E2 activation of ERK1/2 at 10 min, which revealed a PI3K independent activation of ERK at 30 min. Double immunocytochemical labeling for pERK1/2 and pAkt demonstrated that E2 induced both signaling pathways in the same neurons
Slomiany et al., Inflammopharmacology 2006 : The inhibition by PAF antagonist of the LPS induced reduction in mucin synthesis was countered by wortmannin, an inhibitor of PI3K , as well as by ERK inhibitor, PD98059
Pathak et al., J Immunol 2006 : TLR4/PI3K dependent ERK1/2 and p38 MAPK signaling converged upon activation of mitogen- and stress activated protein kinase 1 ( MSK1 )
Vanni et al., Cell cycle (Georgetown, Tex.) 2006 : Furthermore, we investigated the signaling molecules involved in proto-Dbl induced cell transformation and motility and observed that inhibition of PI3K in proto-Dbl expressing cells induces an increase in p38 activity and a decrease in ERK phosphorylation
Cui et al., J Neurochem 2007 : Furthermore, inhibitors of PI3K ( LY294002 and Wortmannin ), MEK1 ( PD98059 and U0126 ), and Src family tyrosine kinases ( PP2 ) decreased IGF-I induced proliferation, and blocked ERK1/2 activation
Cuevas et al., J Hepatol 2007 : Changes in ERK phosphorylation in IRS-4 depleted cells were independent of ras/raf/MEK1/2- and PI3K/Akt-cascades
Wiseman et al., J Immunol 2007 (MAP Kinase Signaling System) : Perforin dependent cryptococcal microbicidal activity in NK cells requires PI3K dependent ERK1/2 signaling
Xu et al., J Cell Biochem 2008 (MAP Kinase Signaling System) : Furthermore, the antiapoptotic effect of lovastatin on mitochondrial apoptotic pathway was effectively abrogated by both PI3K inhibitor, LY294002 and ERK1/2 inhibitor , U0126 ... 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
Boisvert et al., Mol Immunol 2007 : Inhibition studies indicated that activation of ERK and JNK MAPKs and PI3K/AKT are necessary for both TCR- and TCR+alpha2 beta1 integrin dependent IFN-gamma production and that Coll I increases TCR dependent activation of ERK and JNK MAPKs, and AKT
Chuang et al., Endocrinology 2007 (Diabetes Mellitus, Experimental...) : MAPK/ERK inhibitor PD98059 inhibited the PI3K activity, Akt phosphorylation, and lipid accumulation triggered by HG ... PI3K inhibitor LY294002 did not affect the HG-increased ERK1/2 phosphorylation during adipogenesis
Luo et al., Eur J Neurosci 2007 (Optic Nerve Injuries) : In this study we showed that : ( i ) the RGC protection was pathway inhibition dependent ; ( ii ) inhibition of PI3K/akt and JAK/STAT, but not MEK/ERK , activated macrophages in the eye, ( iii ) macrophage removal from the eye using clodronate liposomes significantly impeded PI3K/akt and JAK/STAT inhibition induced RGC survival and axon regeneration whereas it only slightly affected MEK/ERK inhibition dependent protection ; ( iv ) in the absence of recruited macrophages in the eye, inhibition of PI3K/akt or JAK/STAT did not influence RGC survival ; and ( v ) strong PI3K/akt , JAK/STAT and MEK/ERK pathway activities were located in RGCs but not macrophages after ON injury
Liu et al., Am J Physiol Cell Physiol 2007 (Hypertrophy) : Ouabain induced activation of ERK1/2 was prevented by Src, EGFR, and MEK inhibitors, but not by PI3K inhibitors
Kim et al., Biol Pharm Bull 2007 : Water extract of Korean red ginseng stimulates angiogenesis by activating the PI3K/Akt dependent ERK1/2 and eNOS pathways in human umbilical vein endothelial cells ... 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 ... This study demonstrated that KRGE stimulates in vitro and in vivo angiogenesis through the activation of the PI3K/Akt dependent ERK1/2 and eNOS signal pathways and their cross talk
Keum et al., Carcinogenesis 2008 : 3MP-ITC activated ERK1/2 and JNK1/2 and the activation of antioxidant response element ( ARE ) by 3MP-ITC was significantly attenuated by chemical inhibition of PKC and PI3K signaling pathways in HepG2C8 cells
Wagner et al., J Am Soc Nephrol 2007 : Activation of ERK1/2 is partially dependent on PI3-K , and both the PI3-K and MEK-ERK1/2 pathways contribute to PI3-K dependent mitogenesis
Di Fulvio et al., Cell Signal 2008 : PLD2-Y179F caused an increase in phosphorylation of p42/p44 ERK and in the expression of G0/G1 phase transition markers ( p21 CIP, PCNA ), and these effects, too, were dependent on PI3K
Sampaio et al., Mol Cell Biol 2008 : Indeed, by up- and down-regulation of signal strength in different cell lines and through different methods, we observed that Gab1/Shp2 and Ras/ERK1-2 in concert become independent of PI3K upon strong epidermal growth factor receptor (EGFR) stimulation and dependent on PI3K upon limited EGFR activation
Liu et al., PloS one 2007 : We showed that H ( 2 ) O ( 2 ) induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a PI3K inhibitor ( LY294002 ) blocked ERK activation caused by H ( 2 ) O ( 2 ) and a specific inhibitor of MEK ( U0126 ) protected cells from apoptosis
Kondadasula et al., Blood 2008 : Studies with specific chemical inhibitors revealed that the activation of ERK was dependent on the activation of PI3-K , whose activation was dependent on Syk, and that sequential activation of these molecules was required for NK cell IFN-gamma production in response to FcR and IL-12 stimulation
Lee et al., Cell cycle (Georgetown, Tex.) 2008 (Prostatic Neoplasms) : Inhibition of PI3K with either LY294002 and wortmannin was sufficient to cause upregulation of ERK activity as measured by immunoblotting
Bradley et al., J Cell Biochem 2008 : M-CSF activates Ras to coordinate activation of PI3K and Raf/MEK/ERK , since Ras inhibition decreased PI3K activation and PI3K inhibition did not block M-CSF mediated Ras activation
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
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
Palma-Nicolas et al., Biosci Rep 2008 (MAP Kinase Signaling System...) : Pharmacological analysis revealed that the activation of ` conventional ' PKC isoforms is essential for proliferation, although thrombin induced phosphorylation of ERK1/2 requires the activation of atypical PKCzeta by PI3K ... Consistently, thrombin induced ERK1/2 activation and RPE cell proliferation were prevented completely by PI3K or PKCzeta inhibition
Lesma et al., PloS one 2008 (Lymphangioleiomyomatosis...) : In TSC2 ( -/- ) ASM cells specific PI3K inhibitors ( e.g. LY294002, wortmannin ) and Akt1 siRNA had little effect on S6 and ERK phosphorylation
Sun et al., FASEB J 2009 (Inflammation) : Kinetic analysis indicated that PKC isoforms induced early ERK1/2 activation, while PI3K-Akt contributed to the pathway at later time points
Gayer et al., J Biol Chem 2009 : PI3K is required for both ERK and AKT2 activation, whereas AKT2 is sequentially required for GSK-3beta
Gayer et al., Am J Physiol Gastrointest Liver Physiol 2009 (Mechanotransduction, Cellular) : Blocking PI3K prevented strain stimulated ERK and p38 phosphorylation
Ruhland et al., Exp Parasitol 2009 : Interestingly, activation of PI3K/Akt signaling had differential effects on ERK and p38 activation
Wang et al., Molecular systems biology 2009 : We show that, while PI3K signaling is insulated from cross-talk, PI3K enhances Erk activation at points both upstream and downstream of Ras
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
García-García et al., J Immunol 2009 : FcgammaRIIIB induced nuclear phosphorylation of ERK , and of Elk-1, was not affected by Syk, PI3K , or MEK inhibitors
Miller et al., Cancer Res 2009 (Cell Transformation, Neoplastic...) : Oncogenic Kras requires simultaneous PI3K signaling to induce ERK activation and transform thyroid epithelial cells in vivo
Johnson et al., World J Gastroenterol 2009 (Pancreatic Neoplasms) : Inhibition of PI3K with LY294002 suppressed extracellular signal regulated kinase-1 and -2 ( ERK1/2 ) activation in BxPC-3, but enhanced ERK1/2 activation in PANC-1 cells that express IGFBP-5
Fan et al., J Neurosci 2010 : Intracerebroventricular E ( 2 ) infusion also increased PI3K phosphorylation after 15 min, and this effect was blocked by intrahippocampal PI3K, but not ERK , inhibition
Yang et al., Eur J Pharmacol 2010 : 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
Garcia et al., Biochem J 2010 (MAP Kinase Signaling System) : In the present study, we evaluated the role of specific PI3K isoforms alpha, beta, gamma and delta in platelet aggregation, thromboxane A2 generation and ERK ( extracellular-signal regulated kinase ) activation ... Our results show that loss of the PI3K signal impaired the ability of ADP to induce platelet aggregation, ERK phosphorylation and thromboxane A2 generation
Yang et al., J Cell Physiol 2010 (MAP Kinase Signaling System) : Inhibitors of PI3K ( LY294002 and Wortmannin ) prevented the phosphorylation of ERK1/2 , p38 MAPK, and Akt PI3K )
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
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 ... Insulin- or serum induced stimulation of ERK was significantly suppressed by depletion of PI3K-C2a , whereas phosphorylation of IRS-1 and the stimulation of PKB/Akt by insulin were not affected
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 )
Kim et al., Immune network 2011 : Furthermore, PI3-K activity was required for the HBHA induced activation of ERK1/2 and p38 MAPK, but not JNK, pathways
Yen et al., J Biol Chem 2011 (MAP Kinase Signaling System) : PKA, PI3K , and ERK inhibitors abolished PGE2- and cAMP induced c-Fos and MMP-9 up-regulation, and ERK activation was required for the binding of activator protein 1 (AP-1) transcription factor to the MMP-9 promoter
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
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
Kittilson et al., Frontiers in endocrinology 2011 : Although blockade of the ERK pathway had no effect on the activation of Akt, inhibition of PI3K-Akt partially prevented activation of ERK , suggesting cross-talk between the ERK and PI3K-Akt pathways
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 )
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
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
Ha et al., Neurosci Lett 2012 : Furthermore, PI3K activation is responsible for ERK1/2 phosphorylation
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
Boaglio et al., PloS one 2012 (Cholestasis...) : The PI3K inhibitor wortmannin prevented ERK1/2 activation, whereas the cPKC inhibitor Gö6976 prevented p38 activation, suggesting that ERK1/2 and p38 are downstream of PI3K and cPKC, respectively
Chou et al., Toxicol In Vitro 2013 : A specific PI3K inhibitor attenuated the UVB induced ERK1/2 and p53 phosphorylation
Iliev et al., Fish Shellfish Immunol 2013 : The basal phospho-ERK level increased gradually throughout a 5-day culture period and was PI3K dependent as demonstrated by its sensitivity to Wortmannin suggesting it is influenced by growth factors
Marra et al., FEBS Lett 1995 : The results of this study show that in hepatic stellate cells PI 3-K is involved in ERK activation, although it is not necessary
Capodici et al., J Immunol 1998 : Aggregation of human neutrophils is associated with activation of the mitogen activated protein kinases Erk1 and -2, and Erk is activated in response to PI 3-K in some cell types