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PI3 — RELA

Text-mined interactions from Literome

Pan et al., J Biol Chem 1999 (Adenocarcinoma...) : Tumor necrosis factor alpha (TNFalpha) also stimulated increased PI 3-kinase activity, however TNFalpha stimulated NF-kappaB activation was not affected by the PI 3-kinase inhibitors or the p85 dominant negative mutant
Kaliman et al., J Biol Chem 1999 : Regarding the mechanisms involved in IGF-II activation of NF-kappaB, PI 3-kinase inhibition prevented NF-kappaB activation, iNOS expression, and NO production
Sizemore et al., Mol Cell Biol 1999 : In contrast, PI3K inhibitors block the IL-1 stimulated phosphorylation of NF-kappaB itself, especially the p65/RelA subunit
Reddy et al., J Immunol 2000 : Although PI 3-kinase may be required for NF-kappa B activation, overexpression of its p110 catalytic subunit alone was unable to induce an NF-kappa B/chloramphenicol acetyltransferase (CAT) reporter gene
Wooten et al., Mol Cell Biol 2000 : Src, PI3K , and PKC-iota were likewise required for NGF induced NF-kappaB activation and cell survival, whereas Ras was not required for either survival or NF-kappaB activation but was required for differentiation
Guo et al., Inflammation 2000 : IRAK-2 and PI 3-kinase synergistically activate NF-kappaB and AP-1 ... As a result, antisense IRAK-2 ODN or antisense p110 PI 3-kinase ODN inhibited IL-1 induced NF-kappaB and AP-1 activation in HepG2 cells ... These results indicate that IRAK-2 is necessary but insufficient to activate NF-kappaB and AP-1 completely and that although PI 3-kinase is not sufficient for NF-kappaB full activation, it is sufficient to activate AP-1 completely ... The effects of IRAK-2 or PI 3-kinase on NF-kappaB and AP-1 activation were confirmed by the results that overexpression of IRAK-2 failed to fully activate NF-kappaB and AP-1 and that overexpression of p110 PI 3-kinase is insufficient for NF-kappaB full activation but sufficient for AP-1 activation
Wang et al., Biochem Biophys Res Commun 2000 (Colonic Neoplasms) : Taken together, these results suggest that inhibition of PI3-kinase in HT-29 cells results in induction of NF-kappaB binding activity and transactivation which is independent of IkappaBalpha degradation
Koul et al., J Biol Chem 2001 : Taken together, our observations suggest that PI 3-kinase regulates NFkappaB activation through a novel phosphorylation dependent mechanism
Yang et al., J Biol Chem 2001 : Whereas constitutively active PI-3K and Akt induce NF-kappaB activation, Ly294002 ( a PI-3K inhibitor ), dominant negative PI-3K, and kinase-dead Akt block IFN dependent NF-kappaB activation
Guo et al., Acta Pharmacol Sin 2000 (Carcinoma, Hepatocellular...) : To investigate whether phosphatidylinositol (PI) 3-kinase is involved in interleukin-18 (IL-18) induced nuclear factor-kappa B (NF-kappa B) activation ... ( 3 ) Antisense PI 3-kinase ODN inhibited IL-18 induced NF-kappa B activation in a concentration ( 1-8 mg/L ) - and time ( 5-24 h ) -dependent fashion ... PI 3-kinase is necessary for IL-18 stimulated NF-kappa B activation
Funakoshi et al., Int Immunopharmacol 2001 : Above results indicated that both PI3-kinase and p38 MAP kinase are differentially involved in IL-1 induced NF-kappa B and AP-1 activation
Misra et al., Arch Biochem Biophys 2001 (Calcium Signaling...) : We conclude that alpha2M* induced cPLA2 synthesis is controlled by [ Ca2+ ] i levels, tyrosine kinase activity, the p21ras dependent MAPK and PI 3-kinase downstream signaling pathways, and regulation of NFkappaB
Huang et al., J Biol Chem 2001 : We previously demonstrated that fMet-Leu-Phe ( fMLP ) stimulates NF-kappaB activation, and this function of fMLP requires phosphatidylinositol 3-kinase (PI3K)
Reyes-Reyes et al., Biochem J 2002 : However, PI-3K was required for beta1 integrin-, but not beta2 integrin-, mediated NF-kappaB activation ... In addition, inhibition of PI-3K with wortmannin and LY294002 blocked beta1 integrin mediated NF-kappaB activation, but did not affect that mediated by beta2 integrin
Kilpatrick et al., Am J Physiol Cell Physiol 2002 : Inhibition of either PKC-delta or PI 3-kinase attenuated TNF-alpha mediated activation of the antiapoptotic transcription factor NFkappaB
Rahman et al., Circ Res 2002 : Cotransfection of the catalytically inactive Akt mutant inhibited the NF-kappaB activation induced by the constitutively active PI 3-kinase mutant as well as that by the activated forms of Galpha ( q ) and PKC-delta
Ojaniemi et al., Eur J Immunol 2003 : Inhibition of PI 3-kinase decreased the LPS induced transcriptional activity of NF-kappaB, but it had no effect on the nuclear DNA binding activity of NF-kappaB
Das et al., J Biol Chem 2003 (Breast Neoplasms) : However, both pharmacological ( wortmannin and LY294002 ) and genetic ( Deltap85 ) inhibitors of PI 3'-kinase inhibited OPN induced Akt phosphorylation, IKK activity, and NFkappaB activation through phosphorylation and degradation of IkappaBalpha
Hanson et al., J Biol Chem 2003 : The inhibition of NF kappa B is not observed in oncogenic Raf expressing cells and is not fully restored by the suppression of PI3-kinase or MEK pathways
Lee et al., J Biol Chem 2003 : LY294002, dominant negative ( DN ) phosphatidylinositol 3-kinase (PI3K) , or AKT ( DN ) inhibited NFkappaB activation, p65 transactivation, and cyclooxygenase-2 (COX-2) expression induced by lauric acid or constitutively active ( CA ) TLR4
Kang et al., Mol Cell Biochem 2003 : PI3-kinase specific inhibitors, such as wortmannin and LY294003, substantially blocked both silica induced PI3-kinase and NF-kappaB activation ... Antioxidants, such as superoxide dismutase ( SOD ), N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate ( PDTC ), blocked silica induced PI3-kinase activation, suggesting that reactive oxygen species may be important regulatory molecules in NF-kappaB activation by mediating PI3-kinase activation
Li et al., Infect Immun 2003 : Further, these studies suggest that PI3-kinase is an important mediator of LPS and IL-1 beta signaling leading to NF-kappa B activation in endothelial cells and that Akt is necessary but not sufficient for NF-kappa B activation by TLR4
Gustin et al., J Biol Chem 2004 : Pharmacological inhibition of PI 3-kinase blocked TNF induced NF-kappa B DNA binding in the 293 line of embryonic kidney cells, partially affected binding in MCF-7 breast cancer cells, HeLa and ME-180 cervical carcinoma cells, and NIH 3T3 cells but was without significant effect in H1299 and human umbilical vein endothelial cells, cell types in which TNF activated Akt ... Also, inhibitors of PI 3-kinase blocked NF-kappa B DNA binding in Ikk beta-/- but not Ikk alpha-/- or wild-type cells in which the ratio of IKK alpha to IKK beta is low
Bhattacharyya et al., Blood 2004 : Furthermore, IL-10 blocked inducible Akt phosphorylation, and inhibitors of phosphatidylinositol 3-kinase (PI3K) effectively suppressed the activation of Akt, IKK, and NF-kappaB
Kitagawa et al., Am J Physiol Gastrointest Liver Physiol 2004 : Our results indicate that EGF and IL-1beta stimulate two essential signals for iNOS induction in IEC-6 cells : the upregulation of IL-1R1 through PI3-kinase/Akt and the activation of NF-kappaB through IkappaB kinase, respectively
Lubin et al., Neuroscience 2005 : Through inhibition studies we found that extracellular signal regulated protein kinase ( ERK ) and phosphatidylinositol-3 kinase (PI3K) couple to basal and kainate mediated NF-kappaB DNA binding activity in area CA3
Aksoy et al., Eur J Immunol 2005 : In the same models of DC activation, PI3K inhibition increased DNA binding activity of NF-kappaB , but not interferon response factor (IRF)-3, the key transcription factors required for TLR mediated IFN-beta synthesis
Ajuwon et al., J Nutr 2005 : However, the phosphoinositide-3 kinase (PI3K) inhibitor, wortmannin, alone and additively with palmitate, activated the NF-kappaB reporter gene and induced IL-6 expression ( P < 0.05 ). Palmitate also induced the mRNA expression of tumor necrosis factor alpha (TNFalpha) ( P < 0.05 ), but the increase in mRNA abundance was not reflected in a greater protein concentration in the media ( P > 0.05 )
Wang et al., Cancer Res 2005 (MAP Kinase Signaling System) : Because PTEN is a well-known phosphatase involved in the regulation of phosphatidylinositol 3-kinase (PI-3K)/Akt signaling pathway, taken together with the evidence that PI-3K/Akt plays an important role in the activation of AP-1 and NF-kappaB during tumor development, we anticipate that inhibition of AP-1 and NF-kappaB by tumor suppressor p53 seems to be mediated via PTEN, which may be a novel mechanism involved in anticancer activity of p53 protein
Newcomb et al., J Biol Chem 2005 : Inhibition of PI 3-kinase and Akt attenuated RV39 induced NF-kappaB transactivation and IL-8 expression
Bhattacharya et al., Apoptosis 2005 : DN-Akt, as well as the PI3-kinase inhibitors, prevented Akt activation and subsequent translocation of NF-kappaB to the nucleus
Sugimori et al., J Bone Miner Metab 2005 : We investigated the involvement of phosphatidylinositol 3-kinase (PI3K)/Akt mediated NF-kappaB activation by BMP-2 stimulation in the modulation of this antiapoptotic process in a chondrocytic cell line, N1511
Choi et al., Mol Cells 2005 (MAP Kinase Signaling System) : PI3-kinase and PDK-1 regulate HDAC1 mediated transcriptional repression of transcription factor NF-kappaB ... Even though the crucial involvement of the PI3-kinase/Akt pathway in the anti-apoptotic activation of NF-kB is well known, the exact role of PDK-1 as well as PI3-kinase/Akt in NF-kB activation is not understood
Ko et al., FEBS Lett 2005 : Furthermore, PAF induced NF-kappaB activation was blocked by selective inhibitors of Ca ( 2+ ), PI3K , or extracellular signal regulated kinase ( ERK )
Hsieh et al., J Cell Physiol 2006 : Moreover, S1P stimulated activation of NF-kappaB promoter activity was blocked by phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 and helenalin, but not by U0126, suggesting that involvement of PI3K/Akt in the activation of NF-kappaB
Singh et al., Apoptosis 2006 (Histiocytoma) : Inhibition of proteasome activity or its upstream PI3 kinase activity inhibited NFkappaB translocation thereby suppressing apoptosis, which highlights the requirement of NFkappaB activation for completion of apoptosis in AK-5 cells
Nanua et al., Am J Respir Cell Mol Biol 2006 : Quercetin also inhibited TNF-alpha induced PI 3-kinase activity, Akt phosphorylation, intracellular H ( 2 ) O ( 2 ) production, NF-kappaB transactivation , IL-8 promoter activity, and steady-state mRNA levels, consistent with the notion that quercetin inhibits chemokine expression by attenuating NF-kappaB transactivation via a PI 3-kinase/Akt dependent pathway
Kuo et al., Oncogene 2007 : Furthermore, 32D/IRS-1/ALK cells display an enhanced activation of mitogen activated protein kinase and PI3-kinase pathways, and a selective transcriptional activation of nuclear factor (NF)-kappaB
Butler et al., J Biol Chem 2006 : Elafin prevents lipopolysaccharide induced AP-1 and NF-kappaB activation via an effect on the ubiquitin-proteasome pathway
Das et al., Free radical research 2006 (Myocardial Infarction...) : Cardioprotective effect of resveratrol via HO-1 expression involves p38 map kinase and PI-3-kinase signaling, but does not involve NFkappaB
Liu et al., Mol Immunol 2007 : Further studies show that the triptolide mediated inhibitory effects of LPS induced activation of phosphatidylinositol-3 kinase (PI3-K)/Akt and nuclear NF-kappaB activation are involved in down-regulation of COX-2 and CCR7 expression resulting in impaired migration to secondary lymphoid organs of DC
Lalor et al., Ann N Y Acad Sci 2007 (Liver Diseases) : Engagement of VAP-1 results in PI3-kinase dependent NF-kappaB activation and increased chemokine and adhesion molecule expression
Terragni et al., BMC cell biology 2008 : RelB was constitutively bound to promoter regions in cells maintained in serum, however binding decreased following PI 3-kinase inhibition, indicating that PI 3-kinase signaling activates NFkappaB via the non-canonical pathway in proliferating cells
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
Liu et al., Cell Microbiol 2008 (Coxsackievirus Infections...) : However, FRNK transfection and phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 both blocked the IGTP induced translocation and NF-kappaB activation
Liu et al., Mol Immunol 2008 : DNA binding activity of NF-kappaB and phosphorylation of p65 are induced by N-acetylcysteine through phosphatidylinositol (PI) 3-kinase
Kim et al., Toxicological sciences : an official journal of the Society of Toxicology 2009 : The MT-III induced antiapoptotic effects and increase in NF-kappaB activity were blocked by specific inhibitors of TrkA, phosphatidylinositol-3 kinase (PI3K) , Akt, or NF-kappaB, indicating that MT-III provides neuronal protection by activating NF-kappaB through the TrkA/PI3K/Akt signaling pathway
Graham et al., Cancer Sci 2010 (Neoplasm Metastasis...) : We recently reported that phosphoinositide 3-kinase (PI3K)/protein kinase B ( Akt ) mediates transcriptional regulation and activation of bone morphogenetic protein (BMP)-2 signaling by nuclear factor (NF)-kappaB in bone metastatic prostate cancer cells
Lin et al., Virology 2010 (Inflammation...) : ARV S1133 activated PI 3-kinase dependent Akt/NF-kappaB and p70 S6 kinase, as well as Stat3 ; however, p70 S6 kinase was not involved in ARV S1133 mediated effects
Kim et al., Mediators Inflamm 2010 : Immunoblotting analysis suggested that CA inhibition was due to the inhibition of phosphoinositide-3-kinase (PI3K) and phosphoinositide dependent kinase (PDK)1 as well as nuclear factor-(NF-) kappaB activation
Chen et al., J Biol Chem 2010 (Colorectal Neoplasms) : rHSP90alpha induced the activities of ERK, PI3K/Akt , and NF-kappaB p65, but only NF-kappaB activation was involved in HSP90alpha induced integrin alpha(V) expression
Durandy et al., J Immunol 1997 (Hypergammaglobulinemia...) : CD40 triggered activation events, i.e., phosphatidylinositol 3 (PI3) kinase activation and induction of transcription factors NF-kappaB and AP-1, were next analyzed in B cell lines derived from five patients ... Three distinct patterns were observed : an absence of detectable abnormalities ( n = 1 ), defective PI3 kinase activation with normal induction of NF-kappaB and AP-1 ( n = 3 ), and defects in both PI3 kinase activation and induction of NF-kappaB and AP-1 (n = 1)
Reddy et al., J Biol Chem 1997 : Furthermore, two PI 3-kinase-specific inhibitors, wortmannin and a dominant negative mutant of the p85 subunit, inhibited IL-1 induced activation of both NFkappaB and AP-1 ... Our results thus indicate that PI 3-kinase is a novel signal transducer in IL-1 signaling and that it may differentially mediate the activation of NFkappaB and AP-1
Scatena et al., J Cell Biol 1998 : In contrast, inhibition of MEK and PI3-kinase did not affect osteopontin induced NF-kappaB activation
Georgescu et al., Mol Cell Biol 1999 (Cell Transformation, Neoplastic) : On the other hand, we found that both transcriptional activation of NF-kappaB and activation of PI 3-kinase were significantly suppressed with the F867 mutant receptor, suggesting that the activation of antiapoptotic pathways is the major mechanism for the observed phenotypic difference