Gene interactions and pathways from curated databases and text-mining

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HRAS — PI3

Text-mined interactions from Literome

Tanaka et al., J Immunol 1999 (Arthritis, Rheumatoid...) : In this paper we propose that H-Ras mediated activation of PI 3-kinase can be involved in induction of LFA-1 dependent adhesion of T cells, which is relevant to chemokine mediated signaling, and that profilin may form an important link between chemokine- and/or H-Ras mediated signals and F-actin polymerization, which results in triggering of LFA-1 on T cells or leukemic T cells
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
Hart et al., Exp Cell Res 2000 (MAP Kinase Signaling System) : Changes in the actin cytoskeleton, controlled by H-ras61L mediated activation of the Rac/ Rho pathway, as well as PI 3-kinase activation, can also occur in the absence of C-terminal lipid modifications
Tanaka et al., Histol Histopathol 2000 (Inflammation) : We have proposed that H-Ras-sensitive activation of phosphoinositide 3 (PI 3)-kinase and subsequent profilin mediated actin polymerization, can be involved in chemokine induced integrin dependent adhesion of T cells
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
Karasarides et al., J Biol Chem 2001 (Cell Transformation, Neoplastic) : Using an activated Ha-Ras protein ( Y64G/Y71G/F156L ) that fails to interact with PI 3-kinase, we demonstrate that oncogenic Ha-Ras does not require a direct interaction with PI 3-kinase to support anchorage independent growth of IEC-6 epithelial cells
Misra et al., Cell Signal 2001 (MAP Kinase Signaling System) : Thus, COX-2 induction is dependent on cPLA(2) activity, Ca ( 2+ ) mobilization, and PKC activity and requires participation of both the p21(ras) dependent MAPK and PI 3-kinase signalling pathways
Cadwallader et al., J Immunol 2002 : p21(ras) activation ( an upstream regulator of PI3-kinase ) was unaffected by priming
Kaur et al., Biochem J 2006 : As a direct example of pathway networking, Ras-GTP also recruits and activates PI3Ks
Forti et al., An Acad Bras Cienc 2006 (Adrenal Cortex Neoplasms...) : We previously reported that this genetic lesion leads to high constitutive levels of activation of the c-Ki-Ras-GTP -- > PI3K -- > Akt signaling pathway ( Forti et al. 2002 )
Burgering et al., Cell Growth Differ 1994 : To investigate the role of GAP-PI-3K receptor interaction in p21ras signaling, we have used cell lines expressing mutant PDGF receptors that either are impaired in GAP binding or fail to bind both GAP and PI-3K ... These results indicate that binding of GAP and/or PI-3K to the PDGF receptor is not necessary for PDGF induced p21ras activation and p21ras mediated signaling to ERK2 ... We also show that, in contrast to the activation of ERK2, PDGF induced GAP and PI-3K interaction with the PDGF receptor are not inhibited by p21ras ( asn17 ) expression, indicating that these interactions do not require p21ras activation