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EPHB2 — PI3

Text-mined interactions from Literome

Wojtaszewski et al., Am J Physiol 1999 : We conclude that 1 ) insulin and contraction activate ERK signaling in skeletal muscle ; 2 ) ERK signaling is not necessary for activation of glucose and amino acid transport or glycogen synthase activity by contraction and insulin in skeletal muscle ; and 3 ) insulin induced activation of MEK, the upstream activator of ERK, is dependent on PI 3-kinase , whereas contraction utilizes a different mechanism
Sotsios et al., J Immunol 1999 : Hence, it appears that ERK1/2 activation is dependent on PI 3-kinase activation, and both biochemical events are involved in the regulation of SDF-1 stimulated chemotaxis
Parameswaran et al., Eur J Pharmacol 2000 : Thus, these data suggest that activation of ERK by calcitonin gene related peptide involves a H89-sensitive protein kinase A and a wortmannin-sensitive PI3-kinase while activation of p38 MAPK by calcitonin gene related peptide involves only the H89 sensitive pathway and is independent of PI3 kinase
Vacca et al., Cancer Res 2000 (MAP Kinase Signaling System...) : Inhibition by wortmannin of PI3-kinase activity, which has been implicated in ET-1 and other G protein coupled receptor ( GPCR ) -mediated signaling pathways, reduced Erk 2 activation by ET-1 but had no effect on ET-1 induced EGF-R and Shc phosphorylation
Bijur et al., J Neurochem 2000 : Heat shock ( 45 degrees C ) rapidly activated Akt, extracellular signal regulated kinases 1 and 2 ( ERK1/2 ), and p38, but only Akt was activated in a phosphatidylinositol 3-kinase (PI-3K) dependent manner, as the PI-3K inhibitors LY294002 and wortmannin blocked Akt activation, but not ERK1/2 or p38 activation
Kang et al., Mol Pharmacol 2001 : These results demonstrated that t-BHQ activated PI3-kinase and Akt, which was responsible for ARE mediated rGSTA2 induction, and that ERK might negatively regulate rGSTA2 expression, whereas activation of p38 MAP kinase or of JNK by t-BHQ was not associated with the enzyme induction
Suzuma et al., J Biol Chem 2002 : We present novel findings demonstrating that stretch induced VEGF expression in retinal capillary pericytes is mediated by phosphatidylinositol (PI) 3-kinase and protein kinase C (PKC)-zeta but is not mediated by ERK1/2 , classical/novel isoforms of PKC, Akt, or Ras despite their activation by stretch
Bae et al., J Leukoc Biol 2002 : The WKYMVm induced ERK activation was PI 3-kinase dependent but PKC independent
Reyes-Reyes et al., Biochem J 2002 : We found that binding of both types of integrin to their natural ligands activated ERK in a Syk- and PI-3K dependent manner
Jacob et al., J Biol Chem 2002 : Here we demonstrate through the use of PI 3-kinase inhibitors and a dominant negative PI 3-kinase construct that the BCR induced phosphorylation and activation of ERK is dependent on PI 3-kinase
Robin et al., Am J Physiol Cell Physiol 2002 : Inhibition of phospholipase C (PLC) by U-73122 or of phosphoinositide (PI) 3-kinase by wortmannin partially reduced ERK activation
Zhu et al., J Leukoc Biol 2002 : ERK1/2 phosphorylation and eosinophil adhesion were blocked by inhibition of the src-family tyrosine kinase, Janus tyrosine kinase (JAK)2, or phosphoinositide-3 kinase (PI3K)
Nadal-Wollbold et al., FEBS Lett 2002 : This suggests that PI3-kinase was not necessary for ERK2 activation and therefore, that PI3-kinase dependent atypical PKCs were not involved
Bhatt et al., J Immunol 2002 : We found that, in addition to the MAP/Erk kinase inhibitor PD098059, the PI 3-kinase inhibitors LY294002 and wortmannin both suppressed Erk activation in M-CSF treated monocytes, suggesting that 3-phosphorylated products of PI 3-kinase played a role in Erk activation ... These data suggest that, in M-CSF stimulated human monocytes, PI 3-kinase products and ROS production play a role in Erk activation and monocyte survival
Naranatt et al., J Virol 2003 (MAP Kinase Signaling System) : Examination of viral DNA entry suggests a role for PI 3-kinase in HHV-8 entry into the target cells and a role for PKC-zeta, MEK, and ERK at a post-viral entry stage of infection
Feito et al., Eur J Immunol 2003 (MAP Kinase Signaling System) : The association of phosphoinositide 3-kinase (PI-3K) to H4/ICOS was enhanced by H4/ICOS cross linking, and PI-3K inhibitors inhibited ERK and JNK activation and IL-4/IL-10 secretion, but not p38 MAP kinase or ZAP-70 activation
Wilson et al., Invest Ophthalmol Vis Sci 2003 : Fibronectin fragments promote human retinal endothelial cell adhesion and proliferation and ERK activation through alpha5beta1 integrin and PI 3-kinase
Masamune et al., Tohoku J Exp Med 2003 (Fibrosis) : Activation of PI 3-kinase was not required for PDGF-BB induced ERK activation
Opazo et al., J Neurosci 2003 : PI3-kinase inhibitors also block activation of ERK by NMDA receptor stimulation, suggesting that PI3-kinase inhibitors block LTP because PI3-kinase is an essential upstream regulator of ERK activation ... To examine this hypothesis, we investigated the effects of PI3-kinase inhibitors on ERK activation and LTP induction in the CA1 region of mouse hippocampal slices ... Consistent with the notion that ERK activation by NMDA receptor stimulation is PI3-kinase dependent, the PI3-kinase inhibitor wortmannin partially inhibited ERK2 activation induced by bath application of NMDA and strongly suppressed ERK2 activation by high-frequency synaptic stimulation
Rocic et al., Am J Physiol Cell Physiol 2003 (MAP Kinase Signaling System) : This effect was blocked by inhibitors of the ERK1/2 and p38 mitogen activated protein ( MAP ) kinase pathways, but not by PI3-kinase inhibition , and was dependent on PKC, intracellular Ca2+, and tyrosine kinases
Nakayama et al., Biochem Biophys Res Commun 2003 (MAP Kinase Signaling System) : We demonstrated in DC2.4 dendritic cells that ERK regulates tyrosine phosphorylation of phosphatidyl-inositol-3-kinase (PI3-K) and the production of TNF-alpha
Chandrasekher et al., Invest Ophthalmol Vis Sci 2003 : A balance between the nonactivation of PI-3K and the activation of Erk2 may be necessary during early stages of epithelial cell transformation
Schulte et al., Exp Cell Res 2003 : Inhibition of phosphatidylinositol-3'-kinase (PI3K) by wortmannin inhibited adenosine A(2B) receptor mediated ERK1/2 phosphorylation and activation of Rap1, without affecting CREB and p38 phosphorylation
Soldatos et al., Insect Biochem Mol Biol 2003 : Experiments based on inhibitors of specific signaling pathways, such as manumycin A, toxin A, U0126, PD98059 and wortmannin revealed that Ras, MEK and PI-3K are involved in the activation of ERK ... Whether PI-3K is an intermediate of Ras/MEK/ERK pathway or activates ERK via other signaling pathway it remains to be elucidated
Levinthal et al., J Biol Chem 2004 : This study demonstrates that delayed ERK activation is dependent upon the activity of phosphoinositol-3 kinase (PI3K) and that transient but not sustained PI3K inhibition leads to significant protection of neurons from oxidative stress induced neurodegeneration
Ruffels et al., Eur J Pharmacol 2004 (Neuroblastoma) : The phosphatidylinositol 3-kinase (PI-3K) inhibitors wortmannin and LY 294002 ( ( 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ) inhibited H ( 2 ) O ( 2 ) -induced increases in ERK1/2 and PKB phosphorylation
Zhang et al., J Biol Chem 2004 (Carcinoma, Lewis Lung) : Interestingly, suppression of PI 3-kinase signaling by a dominant negative Akt enhanced ERK activity in cells stimulated with 10 ng/ml but not with 100 ng/ml IGF-I
Wandzioch et al., Blood 2004 (MAP Kinase Signaling System) : Surprisingly, phosphoinositide-3 (PI-3) kinase inhibitors block not only PKB/Akt activation but also activation of Raf and Erk ... In mast cells and other more committed hematopoietic precursors, the activation of Erk by SF is not PI-3 kinase dependent
Hassan et al., Regul Pept 2004 (Prostatic Neoplasms) : The effects of NT on EGFR/ERK/Akt activation and DNA synthesis were attenuated by PLC-inhibitor ( U73122 ), PKC-inhibitors ( bisindolylmaleimide, staurosporine, rottlerin ), MEK inhibitor ( U0126 ) and PI3 kinase inhibitors ( wortmannin, LY 294002 )
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 ... 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
Zhuang et al., J Neurosci 2004 (Hyperalgesia...) : Therefore, PI3K induces heat hyperalgesia, possibly by regulating TRPV1 activity, in an ERK dependent manner
Gibbs et al., Int Arch Allergy Immunol 2005 : The IgE dependent release of these mediators in basophils crucially involves PI 3-kinase and the subsequent activation of p38 MAPK and ERK1 & 2
Ghosh et al., Endocr Relat Cancer 2005 (Neoplasms, Hormone-Dependent...) : In a previous report, we showed that increased activation of Akt, a downstream effector of phosphoinositide 3-kinase (PI3K) together with decreased activation of extracellular-signal regulated kinase ( ERK ), a member of the mitogen activated protein kinase ( MAPK ) family, predicted poor clinical outcome in prostate cancer ( Kreisberg et al. 2004 Cancer Research 64 5232-5236 )
Mariappan et al., J Biol Chem 2005 : VEGF induced Erk activation was not dependent on phosphoinositide (PI) 3-kinase activation but required sequential phosphorylation of type 2 VEGF receptor, PLCgamma and c-Src, as demonstrated by inhibitors SU1498, U73122, and PP1, respectively
Jin et al., J Neurosci Res 2005 (MAP Kinase Signaling System) : The phosphatidylinositol 3'-kinase (PI3K) inhibitors LY294002 and wortmannin, and the MAPK/extracellular signal regulated kinase ( ERK ) kinase ( MEK ) inhibitors U0126 and PD98059, reduced HB-EGF induced BrdU incorporation into cultures, and HB-EGF enhanced phosphorylation of Akt and ERK , implying a role for PI3K/Akt and MEK/ERK signaling in HB-EGF stimulated cell proliferation
Kayampilly et al., Endocrinology 2006 : Additionally, inhibition of insulin stimulated PI3 kinase activation reduced ERK phosphorylation
Qiu et al., Int J Oncol 2005 (Ovarian Neoplasms) : Paclitaxel induced ERK and AKT activity was inhibited by the EGFR inhibitor, PD153035 ; ERK inhibitor, U0126 ; and PI3 kinase inhibitor, LY294002, respectively
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
Murata et al., Biochim Biophys Acta 2006 (Leukemia, Monocytic, Acute) : Inhibition of PI3-kinase attenuated VT-1 induced phosphorylation of IKKbeta and ERK2 , and the up-regulation of TF mRNA levels
Punn et al., Mol Endocrinol 2006 : Furthermore, time course studies and use of selective inhibitors demonstrated that ERK1/2 activation occured within 5 min, was sustained for at least 60 min, and was dependent on both phosphatidylinositol 3-kinase (PI3-K)/Akt activation and epidermoid growth factor receptor transactivation involving matrix metelloproteinases
Tchaikovski et al., Arterioscler Thromb Vasc Biol 2008 : PI-3K appears to be a central regulator in VEGFR-1 signaling in monocytes as the activation of Akt, p38, and ERK1/2 are PI-3-K dependent
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
Lin et al., Rheumatol Int 2008 (Chondrosarcoma...) : Using chondrosarcoma cells stimulated with IL-1beta, the effects of GLN on the mRNA and protein levels of MMP-3, the activation of JNK, ERK , p38, NF-kappaB, and AP-1, the nuclear translocation of NF-kappaB/Rel family members, and PI3-kinase/Akt activation were studied
Luke et al., Purinergic Signal 2008 : Inhibitors of protein kinase C ( PKC ), protein kinase A (PKA), Ca ( 2+ ) /calmodulin dependent protein kinase II ( CaMKII ), and phosphoinositide-3 kinase (PI3K) had no effect on ATP mediated ERK1/2 phosphorylation
Tanaka et al., Biochem Biophys Res Commun 2008 : The PAR2 triggered IL-8 release was suppressed by inhibitors of MEK ( U0126 ) or PI3-kinase ( LY294002 ), and PAR2 stimulation indeed activated the downstream kinases, ERK and Akt
Lin et al., Am J Physiol Cell Physiol 2009 (Brain Neoplasms...) : Although both T ( 3 ) and T ( 4 ) stimulated extracellular signal regulated kinase ( ERK ) 1/2, activated ERK1/2 did not contribute to T ( 3 ) -induced Src kinase or PI3-kinase activation, and an inhibitor of PI3-kinase , LY-294002, did not block activation of ERK1/2 by physiological concentrations of T ( 3 ) and T ( 4 )
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
Yu et al., Vascul Pharmacol 2009 (MAP Kinase Signaling System) : TNF-alpha induced apoptosis was significantly decreased by SB203580, a p38 MAPK inhibitor or SP600125, a JNK inhibitor, but was enhanced by an ERK1/2 pathway inhibitor, PD98059 or a PI3-kinase/Akt pathway inhibitor , wortmannin
Banerjee et al., Endocrinology 2009 : This study shows that in the human endometrial cell line, HES, CG, acting via its G-protein coupled receptor, phosphorylates protein kinase B, c-Raf, and ERK1/2 in a phosphatidylinositol 3-kinase (PI3K) dependent manner
Haubner et al., PloS one 2010 (Myocardial Reperfusion Injury) : Mechanistically, PI3Kgamma is required for activation of the Reperfusion Injury Salvage Kinase ( RISK ) pathway ( AKT/ERK1/2 ) and regulates phospholamban phosphorylation in the acute injury response
Kozono et al., Biochem Biophys Res Commun 2010 : CP55940 ( CB1/CB2 agonist ) induced phosphorylation of the extracellular regulated kinases (ERK) 1/2, p38 mitogen activated protein kinase ( p38MAPK ), and Akt in HGFs. Wound closure by CP55940 in an in-vitro scratch assay was significantly suppressed by inhibitors of MAP kinase kinase ( MEK ), p38MAPK, and phosphoinositol 3-kinase (PI3-K)
Park et al., Cardiovasc Res 2011 (Disease Models, Animal...) : Gb3 accumulation reduces K ( Ca ) 3.1 channel expression by down regulating ERK and AP-1 and up-regulating REST and the channel activity by decreasing intracellular levels of PI(3)P
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
Ha et al., Neurosci Lett 2012 : Furthermore, PI3K activation is responsible for ERK1/2 phosphorylation
Marte et al., Curr Biol 1997 (Cell Transformation, Neoplastic) : The constitutive activation of PI 3-kinase alone is sufficient to activate PKB/Akt, but not the MAP kinase ERK or the stress activated protein kinase, Jun N-terminal kinase
Shepherd et al., Diabetologia 1997 : This phosphorylation of p42 ERK2 was not blocked by the PI 3-kinase inhibitors LY294002 and wortmannin although it was blocked by the MAP-kinase kinase ( MEK ) inhibitor PD 98059
Wilden et al., Am J Physiol 1998 : ATP induced activation of ERK1/ERK2 is dependent on the dual-specificity kinase mitogen activated protein kinase/ERK kinase ( i.e., MEK ) but independent of phosphatidylinositol 3-kinase (PI3K) activity