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CRK — 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
Iijima et al., Circulation 2002
:
To elucidate the signaling mechanism underlying the RWP effects, we investigated the effects of RWPs on the activity of
PI3K and the phosphorylation of MAPK pathways in PDGF-BB stimulated SMCs. RWPs
inhibited the PI3K activity and
p38 ( MAPK ) phosphorylation, but not ERK1/2 phosphorylation, in a concentration dependent manner
Strassheim et al., J Immunol 2004
(Inflammation) :
Inhibition of
PI3-K also
prevented activation of
p38 mitogen activated protein kinase and extracellular receptor activated kinase 1/2 in TLR2 stimulated neutrophils
Badr et al., J Immunol 2005
(HIV Infections) :
Unlike CXCL12, gp120 did not
induce the activation of phospholipase Cbeta3 and
PI3K downstream from CXCR4, whereas
p38 MAPK activation was observed
Park et al., Toxicol Appl Pharmacol 2006
(Lymphoma) :
In contrast, the enhanced AP-1 DNA binding activities and
p38 MAPK phosphorylation were significantly
suppressed by specific inhibitors for PKC and p38 MAPK, but not by
PI3-K inhibitors
Hagiwara et al., Nephrol Dial Transplant 2006
(Diabetes Mellitus, Type 2...) :
EPA and specific inhibitors of ERK1/2, JNK and
PI3K decreased levels of MCP-1 in MMCs. EPA
suppressed phosphorylation of ERK1/2 and
p38 in MMCs, and decreased p-ERK positive cells in glomeruli of KKAy/Ta mice
Bouchard et al., Apoptosis 2008
:
Hence, beta1 integrin/Fak/Src signaling translates into integrated mediating functions of
p38beta activation and
regulation of Bcl-2 homologs by
PI3-K/Akt-1 and MEK/Erk, consequently determining their requirement ( or not ) for survival
Wadhone et al., J Immunol 2009
(Leishmaniasis, Visceral) :
Miltefosine induced protein kinase C-dependent and
PI3K dependent
p38MAP kinase phosphorylation and anti-leishmanial function
Bros et al., Gene 2011
:
Both Cacnb3 isoforms, similar to Fscn1, required JNK and
p38 kinase activity for stimulation associated upregulation, and this process was
inhibited by ERK and
PI(3)K
Wang et al., J Cell Mol Med 2012
(Carcinoma, Hepatocellular...) :
Tumour necrosis factor-a (TNF-a) significantly induced phosphorylation of p38 MAPK, ERK, Akt and production of IL-8 from HCC cells, which were prevented by SB203580 (
p38 MAPK inhibitor ), PD98059 ( ERK inhibitor ), LY294002 and Wortmannin (
PI3K inhibitor ) and SB328437 ( CCR3 inhibitor )
Yang et al., Biosci Rep 2012
(Insulin Resistance) :
In contrast, saturated fatty acid exposure caused insulin resistance, reducing
PI3K ( phosphoinositide 3-kinase ) and ERK ( extracellular-signal regulated kinase )
activation while increasing activation of stress kinases JNK ( c-Jun N-terminal kinase ) and
p38