◀ Back to PRKAR1A

PIK3CA — PRKAR1A

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