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PI3 — PIK3R1

Text-mined interactions from Literome

Krasilnikov et al., Biochemistry (Mosc) 2000 (Cell Transformation, Neoplastic...) : The transforming effect of PI3K is supposed to occur on the basis of complex alterations in cellular signaling pathways : appearance of constitutively generated PI3K dependent mitogen signal and activation of some protooncogenes ( src, ras, rac, etc. ), PI3K/PKB-pathway stimulation resulting in delay of apoptosis and increase of cell survival, and actin cytoskeleton reorganization
Ueda et al., Blood 2002 (Calcium Signaling) : In Y719F, the binding of phosphatidylinositol 3'-kinase (PI3K) to KIT was lost and KIT mediated cell migration and Ca ( 2+ ) mobilization were suppressed by PI3K chemical inhibitors or dominant negative PI3K , suggesting the involvement of Y719 mediated PI3K pathway in cell migration
Bilderback et al., Am J Physiol Cell Physiol 2002 : We found that phosphatidylinositol 3-kinase (PI3K) is activated in OSE cells in response to elevated extracellular calcium, and the PI3K inhibitors wortmannin and LY-294002 inhibited extracellular signal regulated kinase ( ERK ) activation by approximately 75 %, similar to effects of the mitogen activated protein kinase/ERK kinase inhibitor PD-98059
Hsu et al., Br J Pharmacol 2003 : 5 Results with specific kinase inhibitors indicate that phagocytic action of PS-G was reduced by the presence of wortmannin ( Phosphatidylinositol 3-kinase , PI3K inhibitor ), pyrazolpyrimidine 2 ( Src-family tyrosine kinase inhibitor ), Ro318220 ( PKC inhibitor ), and SB203580 ( p38 MAPK inhibitor ), but not by PD98059 ( mitogen activated protein/ERK kinase inhibitor )
Perrino et al., J Am Coll Cardiol 2005 (Disease Models, Animal...) : Catalytically inactive PI3KgammaPI3K overexpression in CSQ mice inhibited betaARK1 associated PI3K activity, normalized betaAR levels, and preserved betaAR responsiveness to isoproterenol ( ISO )
Yang et al., J Biol Chem 2005 : In contrast, PI3K does not mediate IFNalpha/beta induced p100 processing, although PI3K is involved in the pathway resulting in IkappaB alpha degradation
Ihle et al., Mol Cancer Ther 2005 (Carcinoma, Non-Small-Cell Lung...) : Recent work shows that phosphatidylinositol-3-kinase (PI3-K) is coupled to the EGFR only in NSCLC cell lines expressing ErbB-3 and that EGFR inhibitors do not inhibit PI3-K signaling in these cells
Caldwell et al., Curr Biol 2005 : Here, we show that the expression of activated Ras, PI3 kinase (PI3K), or Raf specifically in the PG reduces body size, whereas activated Ras or PI3K , but not Raf, increases PG cell size
Guenou et al., Am J Pathol 2006 (Acrocephalosyndactylia) : This was associated with decreased ubiquitin mediated degradation of phosphatidyl inositol 3 kinase (PI3K) and increased PI3K expression and PI3K/Akt signaling
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
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
Xue et al., PloS one 2010 : Phosphatidylinositol 3-kinase (PI3K) activity was also required as indicated by the inhibitory effects of PI3K inhibitors, wortmannin and LY294002, and a PI3K dominant negative ( DN ) mutant Deltap85alpha
Banerjee et al., Mol Cancer Ther 2011 (Disease Models, Animal...) : Third, the incomplete suppression of Nf1-deficient glial cell proliferation in vivo following 5 mg/kg/day rapamycin treatment reflects mTOR mediated AKT activation, such that combined 5 mg/kg/day rapamycin and PI3-kinase (PI3K) inhibition or dual PI3K/mTOR inhibition recapitulates the growth suppressive effects of 20 mg/kg/day rapamycin
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
Bhattacharya et al., Cancer Biol Ther 2012 (Stomach Neoplasms) : In AGS cells, PI3K inhibition alone enhanced 5-FU sensitivity as much as dual PI3K/mTOR inhibition
Tang et al., Cancer Lett 2012 (Bone Neoplasms...) : Activations of phosphatidylinositol 3-kinase (PI3K) , Akt, and AP-1 pathways after HMGB-1 treatment were demonstrated, and HMGB-1 induced expression of integrin and migration activity was inhibited by the specific inhibitor and mutant of PI3K , Akt, and AP-1 cascades
Mohan et al., Science signaling 2013 (Cardiomegaly) : Activation of cardiac phosphoinositide 3-kinase a (PI3Ka) by growth factors, such as insulin, or activation of PI3K? downstream of heterotrimeric guanine nucleotide binding protein ( G protein ) -coupled receptors stimulates the activity of the kinase Akt, which phosphorylates and inhibits glycogen synthase kinase-3 ( GSK-3 )
Fumagalli et al., J Immunol 2013 : These findings suggest that class IA PI3Ks may be activated by PI3K? via Ras in the early phase of the response and by SFKs in the late phase
Glauer et al., Blood cancer journal 2013 : Phosphatidylinositol-3-kinase (PI3K) activation may be associated with tumor progression and drug resistance, and inhibiting PI3K can induce apoptosis in MM cells