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PI3 — RAC3

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
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
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
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
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
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
Nielsen-Preiss et al., Endocrinology 2007 : In addition, PI3K inhibition in GnRH neuronal cells diminished Gas6 induced Rac activation
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
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