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KRAS — PIK3R1
Pathways - manually collected, often from reviews:
-
KEGG Neurotrophin signaling pathway:
HRAS/KRAS/NRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Cholinergic synapse:
PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Regulation of actin cytoskeleton:
HRAS/KRAS/MRAS/NRAS/RRAS/RRAS2
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Aldosterone-regulated sodium reabsorption:
KRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Pathways in cancer:
HRAS/KRAS/NRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Colorectal cancer:
KRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Pancreatic cancer:
KRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Glioma:
HRAS/KRAS/NRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Glioma:
HRAS/KRAS/NRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Melanoma:
HRAS/KRAS/NRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Acute myeloid leukemia:
HRAS/KRAS/NRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Acute myeloid leukemia:
KRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Non-small cell lung cancer:
KRAS
→
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
(protein-protein, activation)
-
KEGG Chemokine signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
TRPV1 (TRPV1)
(modification, activates)
Zhang et al., EMBO J 2005
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
Src (SRC)
(modification, activates)
Zhang et al., EMBO J 2005
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
None
(modification, activates)
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
None
(modification, activates)
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Rodriguez-Viciana et al., Nature 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
RAS family/GTP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
(modification, collaborate)
Rodriguez-Viciana et al., Nature 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
PI3K complex (PIK3CA-PIK3R1)
→
RAS family/GTP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
(modification, collaborate)
Rodriguez-Viciana et al., Nature 1994
Evidence: mutant phenotype, physical interaction
-
WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway:
NRAS/KRAS/HRAS
→
PIK3CA/PIK3R1/PIK3IP1/PIK3R2/PIK3CB/PIK3CD/PIK3R4
(activation)
-
WikiPathways PI3K-AKT-mTOR signaling pathway and therapeutic opportunities:
HRAS/NRAS/KRAS
→
Complex of PIK3CA-PIK3CB-PIK3R1-PIK3R2-PIK3R3-PIK3CG
(activation)
-
WikiPathways Chemokine signaling pathway:
PIK3CA/PIK3CD/PIK3R1/PIK3R2/PIK3R3/PIK3CG/PIK3R5/PIK3CB
→
HRAS/KRAS/NRAS
(activation)
Text-mined interactions from Literome
Amyere et al., Int J Med Microbiol 2002
:
v-Src and
K-Ras activate
PI3K and PLC, as demonstrated by in situ production of the corresponding lipid products
Xu et al., J Biol Chem 2003
(Diabetic Nephropathies) :
Surprisingly, inhibition of
PI3K blocks both ERK and
Ki-Ras activation
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
Shao et al., Cancer Res 2004
(Cell Transformation, Neoplastic...) :
Induction of
K-Ras activated
PI3K and mTOR in IECs
CarĂ³n 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
Staruschenko et al., Biochim Biophys Acta 2005
:
Constitutively active
PI3-K that is incapable of interacting with K-Ras ( K227E p110alpha )
acted as dominant negative with respect to the regulation of ENaC even in the presence of
K-Ras
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 )
Toulany et al., Mol Cancer Res 2007
(Neoplasms) :
Therefore, the role of K-Ras activity for a direct ( i.e., through
activation of
PI3K by
K-Ras ) or an indirect stimulation of PI3K-AKT signaling ( through K-Ras activity dependent EGFR ligand production ) was investigated by means of small interfering RNA and inhibitor approaches as well as ELISA measurements of EGFR ligand production ... Knocking down
K-Ras expression by specific small interfering RNA markedly
affected autocrine production of AREG, but not
PI3K-AKT signaling, after treatment of K-RAS mutated or wild-type cells with EGFR ligands or exposure to ionizing radiation
Rotshenker et al., J Mol Neurosci 2009
(Encephalomyelitis, Autoimmune, Experimental...) :
Observations suggest that Galectin-3/MAC-2 may act as a molecular switch that activates phagocytosis by up-regulating and prolonging
KRas-GTP dependent
PI3K ( phosphatidylinositol 3-kinase ) activity
Miller et al., Cancer Res 2009
(Cell Transformation, Neoplastic...) :
Oncogenic
Kras requires simultaneous
PI3K signaling to induce ERK activation and transform thyroid epithelial cells in vivo
Molina-Arcas et al., Cancer Discov 2013
(Carcinoma, Non-Small-Cell Lung...) :
KRAS is needed for both MEK and PI3K pathway activity in KRAS-mutant, but not wild-type, lung cancer cells, whereas acute activation of
KRAS causes stimulation of
PI3K dependent upon IGF1R kinase activity
Kim et al., Int J Cancer 2013
(Colorectal Neoplasms) :
Taken together, our data suggest that targeting PI3K/MTOR sensitizes cells to apoptosis, implying that
activation of
PI3K/MTOR signaling via
KRAS or PIK3CA mutation is an important pathway in CRC cell growth