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ANXA6 — PI3

Text-mined interactions from Literome

Johanson et al., Exp Cell Res 1999 : The present work shows that thrombin induced p70 ( s6k ) activation is inhibited by the PI 3-kinase inhibitors wortmannin and LY-294002
Rao et al., J Biol Chem 1999 : Whereas inhibition of PI3-kinase by wortmannin completely blocked the p70 ( S6k ) activation, it only partially decreased the ERK2 activity, and had no significant effect on global protein synthesis and bFGF-2 expression induced by PGF2alpha ... These findings demonstrate that 1 ) PI3-kinase dependent and independent mechanisms appear to be involved in PGF2alpha induced activation of ERK2 ; 2 ) PGF2alpha induced eIF4E and 4E-BP1 phosphorylation appear to be mediated by both ERK dependent and PI3-kinase dependent rapamycin-sensitive mechanisms ; and 3 ) ERK dependent eIF4E phosphorylation but not PI3-kinase dependent p70 ( S6k ) activation correlates with PGF2alpha induced global protein synthesis and bFGF-2 expression in VSMC
Brennan et al., Mol Cell Biol 1999 : PI 3-kinase also regulates the activity of p70 ( s6k ), the 40S ribosomal protein S6 kinase, a response that is abrogated by the macrolide rapamycin ... Moreover, the effects of rapamycin on, and the role of p70 ( s6k ) in, IL-2 and PI 3-kinase activation of E2Fs have not been characterized
Weinstein et al., J Leukoc Biol 2000 : Inhibitors of PI 3-kinase or the mammalian target of rapamycin (mTOR) fully blocked p70 S6 kinase activation, implying that this kinase is controlled by PI 3-kinase and mTOR
Guizzetti et al., J Neurochem 2002 (Astrocytoma) : Activation of p70S6K was mediated by M3 muscarinic acetylcholine receptors ( mAChRs ) and was inhibited by two phosphatidylinositol-3-kinase (PI3-K) inhibitors, by a pseudosubstrate to protein kinase C (PKC) zeta, and by the p70S6K inhibitor rapamycin
Le et al., Oncogene 2003 : Inhibitors of mTOR, PI3K , and Ca ( ++ ) impair p70S6K activity, whereas inhibitors of JNK and PKC stimulate p70S6K activity
Ryu et al., J Neurosci Res 2003 : The increase in NSC proliferation observed following ATP application can also be mediated by PI3-kinase dependent p70 S6 kinase activation
Jung et al., Exp Cell Res 2003 (Cell Transformation, Neoplastic...) : While the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 completely abrogated arsenite activation of p70 ( s6k ), ERK1/2 activation by arsenite was not affected by these inhibitors, indicating that H ( 2 ) O ( 2 ) might act as an upstream molecule of PI3K as well as ERK1/2
Kim et al., J Pharmacol Exp Ther 2004 : The phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002 [ 2- ( 4-morpholinyl ) -9-phenyl-4H-1-benzopyran-4-one ], dominant negative Akt, or rapamycin, an inhibitor of mTOR ( mammalian target of rapamycin ) and ribosomal p70 S6 kinase (p70S6K) phosphorylation, inhibited the insulin mediated increase in GCLC protein and GSH levels
Banno et al., J Biol Chem 2005 : H ( 2 ) O ( 2 ) -induced phosphorylation of Akt and p70S6K was dependent on phosphatidylinositol 3-kinase (PI3K) activity and was abolished by 1-butanol but not t-butanol
Le Pabic et al., J Hepatol 2005 : The phophatidylinositol 3-kinase (PI3K) inhibitor LY294002 and the mitogen activated protein kinase inhibitor, UO126, decreased the TGF-beta1 dependent ADAM12 expression and prevented the phosphorylation of p70S6K
Kim et al., J Pharmacol Exp Ther 2006 : Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [ 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant negative and kinase-dead Akt, effectively inhibited the insulin mediated increase in alpha-class GST expression and GST activity toward NBD
Belham et al., Cell Signal 1997 : The phosphatidylinositol (PI) 3-kinase inhibitor wortmannin also completely blocked p70s6k activity in response to thrombin but did not affect p70s6k activity evoked by platelet derived growth factor ( PDGF ) at a concentration that abrogated PDGF stimulated PI 3-kinase activity
Lin et al., J Biol Chem 1997 : The role of PI 3-kinase in regulating heat shock activation of MAPK and p70 S6K was investigated using wortmannin, a specific pharmacological inhibitor of PI 3-kinase
Rousse et al., Endocrinology 1998 : Because the PI3-kinase inhibitors block p70S6k , neither kinase would be required for IGFR-1 dependent IGFBP-5 induction
Tudan et al., Biochem J 1998 : This crystal induced activation of p70 ( S6K ) could also be inhibited by a protein kinase C ( PKC ) inhibitor ( Compound 3 ), but not by the PI 3-kinase inhibitor wortmannin
Schuppin et al., Diabetes 1998 (Insulinoma...) : This serum stimulated DNA synthesis was prevented by inhibitors of tyrosine protein kinase and phosphatidylinositol (PI) 3-kinase activities, as well as the activation of mitogen activated protein ( MAP ) kinase and p70S6K
Hügl et al., J Biol Chem 1998 : Thus, glucose and IGF-I induced beta-cell proliferation were mediated via a signaling mechanism that was facilitated by mitogen activated protein kinase but dependent on IRS mediated induction of PI 3'-kinase activity and downstream activation of p70 ( S6K )
Ge et al., Biochem Biophys Res Commun 1998 : In addition, wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI-3-K) , rapamycin, an inhibitor of p70 ( S6K ) and PD 098059, an inhibitor of mitogen activated protein kinase ( MAPK ) kinase were able to inhibit AII induced enhanced expression of Gialpha-2 and Gialpha-3 to various degrees