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PI3 — RAC1

Text-mined interactions from Literome

Beeton et al., Mol Cell Biol Res Commun 1999 : However, the ability of activated Rac to stimulate PI 3-kinase activity was only observed in heterodimers containing the p85alpha and deltaSH3-p85alpha, indicating that rac binding to the BH domain is responsible for rac induced stimulation of class Ia PI 3-kinase
Gille et al., J Biol Chem 1999 : Activated PI 3-kinase induces cyclin D(1) transcription and E2F activity, at least in part mediated by the serine/threonine kinase Akt/PKB, and to a lesser extent the Rho family GTPase Rac
Katagiri et al., Mol Cell Biol 2000 : H-Ras and Rac activated LFA-1 in a PI 3-kinase dependent manner, whereas Rho and R-Ras had little effect
Banyard et al., Oncogene 2000 : We also show that constitutively active V12-Rac significantly stimulated basal Rat1 fibroblast invasion, independent of PI-3-kinase activity, and that this effect was suppressed by the effector mutant V12/H40-Rac
Sanlioglu et al., J Virol 2000 : Inhibition of Rac1 using a dominant N17Rac1 mutant led to a decrease in AAV-2 mediated PI3 kinase activation, indicating that Rac1 may act proximal to PI3 kinase during AAV-2 infection
Storey et al., Curr Biol 2002 : Rho stimulation by G ( 13 ) -coupled receptors and Rac stimulation by nuclear hormones through PI3-kinase may be general mechanisms for regulating ion channel activity in many cell types
Arai et al., Oncogene 2002 : In addition, the cytokine induced Rac activation was inhibited by a phosphatidyl-inositol 3'-kinase (PI3K) inhibitor, LY294002, which also inhibited the Erk activation
Yamamori et al., Biochem Biophys Res Commun 2002 : Phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002, blocked not only p38 MAPK activation but also Rac activation
Lee et al., J Biol Chem 2003 (Carcinoma, Hepatocellular) : The exact link between selenite treatment, Rac1 activation , and activation of the focal adhesion kinase-PI 3-kinase , however, remains to be characterized
Marcoux et al., Oncogene 2003 : Our further functional studies identified Vav2, a known exchange factor for Rac, as a crucial downstream component in EGFR- and PI 3-kinase dependent Rac activation upon integrin mediated cell adhesion
Brantley-Sieders et al., J Cell Sci 2004 (Neovascularization, Pathologic) : Ephrin-A1 stimulation induces PI3-kinase dependent activation of Rac1 in wild-type endothelial cells, whereas EphA2-deficient cells fail to activate Rac1 upon stimulation
Felekkis et al., Mol Cancer Res 2005 (Breast Neoplasms) : As phosphatidylinositol 3-kinase (PI3K) signaling can regulate Rac activation, we examined the effects of AND-34 on PI3K
Vecchione et al., J Exp Med 2005 (Hypertension) : In response to angiotensin II, PI3Kgamma was required for the activation of Rac and the subsequent triggering of ROS production
Pan et al., J Neurochem 2005 : RA-induced activation of Rac1 is mediated by phosphatidylinositol 3-kinase (PI3K) , probably because of phosphorylation of the p85 regulatory subunit by Src kinases
Vedham et al., Mol Cell Biol 2005 : We conclude that Vav acts as a PI 3-kinase dependent activator for Rac activation in macrophages stimulated with M-CSF and that SHIP regulates macrophage M-CSF triggered chemotaxis by hydrolysis of PI ( 3,4,5 ) P ( 3 )
Di Marzio et al., Biochem Biophys Res Commun 2005 : Moreover, this MIP-1alpha induced Rac activation and consequent lamellipodia formation is Gi- and phosphoinositide-3 kinase (PI3K) mediated
Alblas et al., Mol Cell Biol 2005 : Furthermore, SIRPalpha induced NO production required the generation of hydrogen peroxide ( H ( 2 ) O ( 2 ) ) by a NADPH oxidase ( NOX ) and the phosphatidylinositol 3-kinase (PI3-K) dependent activation of Rac1 , an intrinsic NOX component
Park et al., Cancer Res 2005 (Fibrosarcoma...) : Consistent with the increased cell migration/invasion of syndecan-2 overexpressing HT1080 cells, syndecan-2 overexpression increased phosphorylation and interaction of focal adhesion kinase ( FAK ) and phosphatidylinositol 3-kinase (PI3K) , membrane localization of T-lymphoma invasion and metastasis gene-1 ( Tiam-1 ), and activation of Rac
Gonzalez et al., J Biol Chem 2006 : Taken together, these studies identify G protein betagamma subunits, Src kinase and the GEF Tiam1 as upstream modulators of S1P mediated Rac1 activation, and establish a central role for Rac1 in S1P mediated activation of PI 3-kinase/Akt/endothelial nitric-oxide synthase signaling in vascular endothelial cells
Seveau et al., Cell Microbiol 2007 : PI 3-kinase activation was upstream and independent of Rac1 activation
Nielsen-Preiss et al., Endocrinology 2007 : In addition, PI3K inhibition in GnRH neuronal cells diminished Gas6 induced Rac activation
Aoki et al., J Cell Biol 2007 : Further refinement of the computational model predicted Rac1 regulation of PI3-kinase and SHIP2, which was also validated experimentally
Jin et al., Neurochem Int 2007 : These results suggest that the NGF induced ruffling requires activation of Rac1 and Cdc42, but does not require Ras, PI-3k , Akt and GSK-3beta
Yip et al., J Cell Sci 2007 (Adenocarcinoma) : Both Rac and Ras have been shown to regulate actin polymerization and activate PI 3-kinase
Leventhal et al., Trends Endocrinol Metab 1997 : This effect of the IGFs is mediated by activation and autophosphorylation of the type I IGF receptor, followed by docking of insulin receptor substrate-1 (IRS-1), stimulation of phosphatidylinositol (PI) 3-kinase , and possibly activation of the small GTPase Rac
Hubchak et al., American journal of physiology. Renal physiology 2009 (Fibrosis) : Rac1 activation required phosphatidylinositol-3-kinase (PI3K) activity
Xia et al., Journal of thrombosis and haemostasis : JTH 2010 : Subsequently, PI3K overexpression activated Rac1 and increased ROS generation
Jeanes et al., J Mol Histol 2009 : This is independent of potential effects on adhesion or polarity, but may occur through PI3-kinase stimulated Rac signaling
Zhang et al., J Cell Mol Med 2011 (Endotoxemia...) : The aim of this study was to investigate the role of Rac1 in TNF-a expression and cardiac dysfunction during endotoxemia and to determine the involvement of phosphoinositide-3 kinase (PI3K) in lipopolysaccharide (LPS) induced Rac1 activation
Kim et al., Exp Mol Med 2012 (Diabetes Mellitus, Experimental...) : The phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin, simultaneously regulates Rac1 and Cdc42, which destabilize the podocyte actin cytoskeleton during early DN
Koch et al., Neurobiol Dis 2013 : This correlates with the reggie-1 dependent activation of Src and PI3 kinase (PI3K) , of the Rho family GTPase Rac1 and downstream effectors such as cofilin
Spillane et al., J Neurosci 2012 : The effects of NGF on Rac1 activity and increases in axonal levels of WAVE1 and cortactin were both dependent on phosphoinositide 3-kinase (PI3K) signaling
Basquin et al., Communicative & integrative biology 2013 : Thus, PI3K regulates both the activation of Rac1 and its recruitment during IL-2R endocytosis
Zheng et al., J Biol Chem 1994 : These findings suggest that PI 3-kinase , through the Rho-GAP homology domain of p85, can couple to the effector domain of Cdc42Hs and that p85 may be a target for the GTP bound forms of Cdc42Hs and Rac1