Gene interactions and pathways from curated databases and text-mining

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AKT1 — PRKACB

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Filippa et al., Mol Cell Biol 1999 : In this report, we show that PKB can also be activated by PKA ( cyclic AMP [ cAMP ] -dependent protein kinase ) through a PI3-kinase independent pathway ... Although this activation required phosphorylation of PKB, PKB is not likely to be a physiological substrate of PKA since a mutation in the sole PKA consensus phosphorylation site of PKB did not abolish PKA induced activation of PKB ... We looked at events downstream of PKB and found that PKA activation of PKB led to the phosphorylation and inhibition of glycogen synthase kinase-3 ( GSK-3 ) activity, a known in vivo substrate of PKB ... However, high concentrations of wortmannin did not abolish PKB activation, which demonstrates that translocation per se is not important for PKA induced PKB activation
Tsygankova et al., Mol Cell Biol 2001 : Although the expression of activated Rap1A was sufficient to stimulate wortmannin-sensitive Akt phosphorylation, TSH further increased Akt phosphorylation in a phosphatidylinositol 3-kinase- and PKA dependent manner
Mei et al., J Biol Chem 2002 : Activation of Epac leads to a phosphatidylinositol 3-kinase dependent PKB activation, while stimulation of PKA inhibits PKB activity ... The opposing effects of Epac and PKA on PKB activation provide a potential mechanism for the cell type-specific differential effects of cAMP
Trümper et al., J Endocrinol 2002 (MAP Kinase Signaling System) : These interactions included : ( i ) a central role of tyrosine phosphorylation for stimulation of PKA/CREB, MAPK and PI3-kinase/PKB, ( ii ) inhibition of PKA/CREB by the MAPK pathway at the level of MAPK kinase-1 or downstream, ( iii ) activation of MAPK signaling by PI3-kinase and PKA at the level of extracellular-signal regulated kinase 1/2 or upstream, and ( iv ) activation of PKB by MAPK and PKA signaling at the level of PKB or upstream
Schmitt et al., J Biol Chem 2002 (MAP Kinase Signaling System) : In contrast, the activation by isoproterenol of Ras requires Gbetagamma subunits, is independent of PKA , and results in the phosphoinositol 3-kinase dependent activation of AKT
Cullen et al., Am J Physiol Gastrointest Liver Physiol 2004 : The role of cAMP-GEF and PKA on activation of Akt , a kinase implicated in cAMP survival signaling, was investigated
Brennesvik et al., Cell Signal 2005 : Inhibition of PKA by H89 decreased adrenaline stimulated glycogen phosphorylase activation but increased PKB activation, which further supports that adrenaline increases insulin stimulated PKB phosphorylation via Epac
Misra et al., J Cell Biochem 2007 : The PKA inhibitor H-89, greatly attenuated forskolin induced Akt1 synthesis
Hong et al., J Biol Chem 2008 : Here we show that ( i ) upstream regulators, PIK and PDK1, are not the target ( s ) of the cAMP inhibitory action ; ( ii ) constitutively active Akt and calyculin A-stimulated Akt are resistant to cAMP inhibition, suggesting the action of a phosphatase ; ( iii ) cAMP increases the rate of Akt dephosphorylation, directly implicating an Akt-phosphatase ; ( iv ) Epac- and protein kinase A (PKA)-specific analogs synergistically inhibit Akt, indicating the involvement of both cAMP dependent effector pathways ; ( v ) H89 and dominant negative Epac 279E block cAMP-inhibitory action ; ( vi ) Epac associates in a complex with Akt and PP2A, and the associated-phosphatase activity is positively modulated by cAMP in a PKA- and Rap1 dependent manner ; ( vii ) like its action on Akt inhibition, PKA- and Epac-specific analogs synergistically activate Epac associated PP2A ; and ( viii ) dominant negative PP2A blocks cAMP-inhibitory action
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
Bellis et al., Arterioscler Thromb Vasc Biol 2009 (Disease Models, Animal...) : In addition, in early and late PC, PKA physically interacted with the phosphorylated form of Akt, suggesting that PKA is required for Akt phosphorylation ... Late ischemic PC protects BAECs against hypoxia through PKA- and PI3K dependent activation of Akt
Baviera et al., Mol Cell Endocrinol 2010 : On the other hand, inhibition of PKA by H89 further increased the phosphorylation levels of AKT and Foxo3a induced by epinephrine, DBcAMP or 8CPT-2Me-cAMP
Hu et al., Acta Pharmacol Sin 2010 (Pancreatic Neoplasms) : Activation of beta-AR receptor transactivates epidermal growth factor receptor (EGFR) and then elicits Akt and ERK1/2 in a PKA dependent manner, which together up-regulate levels of HIF-1alpha and downstream target genes independently of oxygen level
Choi et al., Mol Cell Biol 2010 (Insulin Resistance) : Furthermore, insulin regulates total PKA activity in an Akt dependent manner
McDougall et al., Synapse 2011 : PKA activity of Mn-treated rats was enhanced in both the dorsal striatum and PFC, whereas p-Akt levels were elevated in the dorsal striatum
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
Wang et al., BMC cancer 2012 : PKA activation in TG2 overexpressing MEF ( tg2-/- ) cells resulted in an increased activation of NF-?B and Akt phosphorylation in comparison to empty vector transfected control cells as determined by the reporter-gene assay and immunoblot analysis respectively
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
Balwani et al., PloS one 2012 : Thus, MPTAG mediated inhibition of TNF-a induced Akt activation was independent of PI-3K and dependent on PKA ... Most importantly, MPTAG restores the otherwise repressed activity of PKA and inhibits the TNF-a induced Akt phosphorylation at both Thr308 and Ser473 residues