◀ Back to PIK3R1
PIK3R1 — RHOA
Pathways - manually collected, often from reviews:
-
NCI Pathway Database LPA receptor mediated events:
RHOA/GTP complex (RHOA)
→
PI3K-beta complex (PIK3CB-PIK3R1)
(modification, activates)
Baudhuin et al., Mol Pharmacol 2002*
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
PI3K complex (PIK3CA-PIK3R1)
→
RHOA/GDP complex (RHOA)
(modification, activates)
Cozzolino et al., Mol Biol Cell 2003
Evidence: mutant phenotype
-
NCI Pathway Database SHP2 signaling:
PI3K complex (PIK3CA-PIK3R1)
→
RHOA/GTP complex (RHOA)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database S1P2 pathway:
RhoA (RHOA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
Sugimoto et al., Mol Cell Biol 2003, Arikawa et al., J Biol Chem 2003, Gonda et al., Biochem J 1999
-
NCI Pathway Database IL2-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
RHOA/GTP complex (RHOA)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997, Gadina et al., J Immunol 1999
Evidence: mutant phenotype, assay, physical interaction, other species
-
NCI Pathway Database Osteopontin-mediated events:
Rho Family GTPase-active (RHOA/CDC42/RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Biswas et al., BMC cell biology 2004*, Chellaiah et al., Mol Biol Cell 1996
Evidence: mutant phenotype, assay
Text-mined interactions from Literome
Cozzolino et al., Mol Biol Cell 2003
:
The deleted mutant also inhibits the
PI3K dependent
RhoA activation ensuing receptor activation
Viswambharan et al., Circ Res 2004
:
In conclusion, rHDL inhibits thrombin induced human endothelial TF expression through inhibition of
RhoA and
activation of
PI3K but not Akt/eNOS
Jiang et al., Mol Cell Biol 2004
(Cell Transformation, Neoplastic...) :
Ectopic expression of RhoB, but not the close relative
RhoA ,
inhibits Ras,
PI3K , and Akt induction of transformation, migration, and invasion and induces apoptosis and anoikis
Teusch et al., J Immunol 2004
:
In contrast to previous studies, identifying Rac1-PI3K as an upstream element in TLR2 initiated response to NF-kappaB,
PI3K signaling was not
required for
RhoA or PKCzeta activity
Da Silva et al., Nat Neurosci 2005
:
PMGS induces axon specification by enhancing TrkA activity locally, which triggers phosphatidylinositol-3-kinase
(PI3K)- and Rac1 dependent
inhibition of
RhoA signaling and the consequent actin depolymerization in one neurite only
Raghu et al., J Virol 2007
(Herpesviridae Infections) :
RhoA-GTPase activation was
inhibited by
PI3-K inhibitors, demonstrating that PI3-K is upstream to RhoA-GTPase
Meng et al., Br J Cancer 2009
(Adenocarcinoma...) :
The
PI3K inhibitor, LY294002, further
blocked the expression of MMP9 and
RhoA
Tiwari et al., J Gen Virol 2010
:
We also show that inhibition of
PI3K signalling also
affected RhoA activation required for HSV-1 entry into certain cell types
Zeidan et al., Mol Cell Biochem 2011
:
Our results demonstrate a critical
role for
PI3K/mTOR/p70 ( S6K ) in leptin induced
RhoA activation resulting in cardiomyocyte hypertrophy associated with GATA4 stimulation
Liu et al., Cell Signal 2013
(Stomach Neoplasms) :
PI3K/Akt dependent phosphorylation of GSK3ß and activation of
RhoA regulate Wnt5a induced gastric cancer cell migration