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AKT1 — PRKAR1B
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