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PIK3CA — PRKAR2A
Text-mined interactions from Literome
Carini et al., Gastroenterology 2004
(Reperfusion Injury) :
In the cells treated with CGS21680,
PI3K activation was
prevented either by inhibiting adenylate cyclase and
PKA with, respectively, 2,5-dideoxyadenosine and H89 or by blocking Galphai-protein and Src tyrosine kinase with, respectively, pertussis toxin and PP2 ...
PI3K is
activated following hepatocyte hypoxic preconditioning by the combined stimulation of adenosine A 2A receptors,
PKA , Galphai protein, and Src
Leblais et al., Circ Res 2004
(Calcium Signaling...) :
These results suggest that beta1-AR stimulation activates PI3K via a PKA dependent mechanism, and that G ( betagamma ) and the subsequent activation of betaARK1 are critically involved in the
PKA induced
PI3K signaling which, in turn, negates cAMP induced positive inotropic effect via inhibiting sarcolemmal Ca2+ influx and the subsequent increase in intracellular Ca2+ transients, without altering the receptor mediated phospholamban phosphorylation, in intact cardiomyocytes
De Gregorio et al., Oncogene 2007
:
We suggest that ( 1 ) TSH-cAMP induced
PKA phosphorylates p85alpha ( PI3K ) at serine 83, ( 2 ) phosphorylated p85alpha ( PI3K ) binds RIIbeta-PKA and targets PKAII to the membrane, and ( 3 ) PI3K activity and p21Ras binding to PI3K increase and
activate PI3K downstream targets
Park et al., Biochem Biophys Res Commun 2009
:
HO-1 expression by PGE ( 2 ) was inhibited by LY294002,
PI3K inhibitor and H89,
PKA inhibitor
Namkoong et al., Cell Signal 2009
:
Forskolin increases angiogenesis through the coordinated cross-talk of
PKA dependent VEGF expression and Epac mediated
PI3K/Akt/eNOS signaling ... These results suggest that forskolin stimulates angiogenesis through coordinated cross-talk between two distinct pathways,
PKA dependent VEGF expression and Epac dependent ERKactivation and
PI3K/Akt/eNOS/NO signaling
Yan et al., FASEB J 2011
:
The antimitogenic efficacy of PGE ( 2 ) in inhibiting control cultures was associated with greater ability to stimulate sustained
PKA activation and greater
inhibition of late-phase promitogenic p42/p44 and
PI3K activities
Makarova et al., J Biol Chem 2011
(Acute Lung Injury...) :
uPA induced phosphorylation of eNOS was also inhibited by the
protein kinase A (PKA) inhibitor, myristoylated PKI, but was not
dependent on
PI3K-Akt signaling
Nascimento et al., Eur J Pharmacol 2012
:
Relaxin induced AKT phosphorylation was G ( i ) - but not
PKA dependent , and it was blocked by both
PI3K and MEK inhibitors