Gene interactions and pathways from curated databases and text-mining

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HRAS — PIK3CA

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Madrid et al., Mol Cell Biol 2000 : In this study, we show that oncogenic H-Ras requires PI3K and Akt to stimulate the transcriptional activity of NF-kappaB
Guillemot et al., J Biol Chem 2001 (MAP Kinase Signaling System) : Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a p21(ras)/Raf-1/MEK/ERK dependent manner, and also involves PI3K and SHP-2
Weber et al., Mol Biol Cell 2001 : Our data suggest that inhibition of initial PI3-K activation by inactive H-Ras or sustained activation of an inhibitory ERK pathway by active H-Ras prevail to abolish LFA-1 regulation and transendothelial migration induced by SDF-1alpha in leukocytes, establishing a complex and bimodal involvement of H-Ras
Choi et al., Oncogene 2004 : Taken together, these findings explain the opposite effects of Ha-Ras and Ki-Ras on modulation of radiosensitivity, and suggest that differential activation of PI3K/Akt and Rac/p38 MAPK signaling by Ha-Ras and Ki-Ras may account for the opposing response to the ionizing radiation
Carón et al., Mol Cancer Ther 2005 (Carcinoma...) : In HCT116 cells expressing H-RAS V12, PI3K dependent radioresistance is mediated by both H-RAS dependent translocation of PI3K into the plasma membrane and heregulin induced activation of membrane localized PI3K via ERBB3
Carón et al., Mol Cancer Ther 2005 (Carcinoma...) : Activated forms of H-RAS and K-RAS differentially regulate membrane association of PI3K , PDK-1, and AKT and the effect of therapeutic kinase inhibitors on cell survival
David et al., J Immunol 2005 : In that pharmacological inhibitors of PI3K inhibited LPS induced activation of p21Ras , but not activation of ERK, we concluded that LPS induced activation of ERK occurs through a pathway that is not dependent on the activation of p21Ras
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 )
Yoon et al., Mol Cancer Ther 2006 (Breast Neoplasms...) : H-Ras did not increase MMP-9 in the presence of a PI3K inhibitor, LY294002, and a NF-kappaB inhibitor, SN50
Fivaz et al., Curr Biol 2008 : Here, we use live FRET imaging in hippocampal neurons and show that the activity of the small GTPase HRas , an upstream regulator of PI3K , markedly increases in the nascent axonal growth cone upon symmetry breaking