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GSK3B — PRKAR1A

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PRKAR1A — GSK3B (physical association, affinity chromatography technology) Varjosalo et al., Nat Methods 2013
• IRef Intact Interaction: Complex of 12 proteins (association, tandem affinity purification) Varjosalo et al., Cell reports 2013

Text-mined interactions from Literome

Luo et al., J Alzheimers Dis 2004 : Independent of these effects, inhibition of PKA by H89 ( 10 uM ) significantly blocked TRH inhibition of GSK-3 beta
Jensen et al., Cell Signal 2007 : The PKA inhibitor H89 ( 50 microM ) reduced adrenaline stimulated GSK-3beta Ser9 phosphorylation but did not influence the effects of insulin
O'Driscoll et al., J Neurochem 2007 : The effects of bFGF on GSK3beta were dependent on protein kinase A (PKA) activation, as inhibition of this pathway blocked inactivation
Torii et al., Cell Signal 2008 : Based on another finding indicating that Wnt5a upregulated PKA mediated phosphorylation of glycogen synthase kinase-3beta ( GSK-3beta ) at serine 9 that caused inactivation of GSK-3beta and subsequently resulted in activation of the beta-catenin pathway, we have speculated that the Wnt5a anti-apoptotic activity may be partially mediated by PKA mediated phosphorylation of GSK-3beta and subsequent activation of the beta-catenin pathway
Hayashi et al., Thromb Haemost 2009 : These results suggested that cAMP elevating agents have two effects on PI3K signalling : inhibition of Akt phosphorylation independent of PKA ; and stimulation of GSK-3beta phosphorylation dependent on PKA