Gene interactions and pathways from curated databases and text-mining

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GSK3B — PIK3R1

Pathways - manually collected, often from reviews:

  • KEGG Influenza A: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → GSK3B (protein-protein, inhibition)

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Lenferink et al., Cancer Res 2001 (Breast Neoplasms...) : The inhibition of PI3K/Akt resulted in increased activity of glycogen synthase kinase-3beta , which phosphorylated cyclin D1, potentially reducing its steady-state levels
Hetman et al., J Biol Chem 2002 : Here, we report that inhibition of ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and PI3K were required for brain derived neurotrophic factor (BDNF) suppression of GSK3beta activity ... Although both PI3K and ERK1/2 inhibited GSK3beta activity, neither had an effect on GSK3beta phosphorylation at Tyr-216 ... Interestingly, PI3K ( but not ERK1/2 ) induced the inhibitory phosphorylation of GSK3beta at Ser-9
Desbois-Mouthon et al., Hepatology 2002 (Carcinoma, Hepatocellular...) : By using LY294002 and ML-9, which act as phosphatidylinositol 3-kinase (PI3-K) and Akt inhibitors, respectively, we showed that GSK-3beta phosphorylation required PI3-K activation in both cell lines whereas downstream Akt activation was required only in Mahlavu cells
Ma et al., Biochem Pharmacol 2004 : Furthermore, DEP promoted phosphorylation of Akt, a substrate of phosphatidylinositol 3-kinase (PI3K), on Ser-473 and Thr-308 in a PI3K dependent manner, and enhanced phosphorylation of down-stream p70/p85 S6 kinases ( p70/p85S6K ) as well as glycogen synthase kinase-3beta ( GSK-3beta )
Beurel et al., Int J Oncol 2005 (Carcinoma, Hepatocellular) : Therefore, PI3K mediated GSK-3beta inhibition could be a mechanism by which cancer cells escape from chemotherapy induced apoptosis
Wong et al., Life Sci 2005 (Enterovirus Infections) : The activity of GSK3beta , a downstream target of these pathways, was negatively regulated by the activation of both MAPK/ERK and PI3K/Akt
Rajala et al., J Virol 2005 : We demonstrate phosphorylation of GSK-3beta and nuclear translocation of the p65 subunit of NF-kappaB, both downstream targets of the PI3K/Akt pathway, in adenovirus infected corneal fibroblasts in a PI3K dependent manner
Almeida et al., J Biol Chem 2005 : Wnt3a induced phosphorylation of GSK-3beta and downstream activation of beta-catenin mediated transcription required ERK, PI3K , and Akt signaling
Xu et al., J Cell Biochem 2008 (MAP Kinase Signaling System) : The activation of ERK1/2 was inhibited by a PI3K inhibitor, LY294002, but U0126, a ERK1/2 inhibitor did not inhibit phosphorylation of Akt and GSK3 beta
Yu et al., J Neurochem 2008 : Moreover, SKF83959 treatment significantly inhibited H2O2 activated glycogen synthase kinase-3beta ( GSK-3beta ) which was associated with the drug 's neuroprotective effect, but this inhibition was attenuated by SCH23390 and a selective PI 3-K inhibitor
Nishimoto et al., J Neurosci Res 2008 (Brain Ischemia...) : These findings suggest that AMPA activates PI3K-Akt and subsequently inhibits GSK3beta and that inactivated GSK3beta attenuates glutamate induced caspase-3 cleavage and neurotoxicity
Yoon et al., Biochem Biophys Res Commun 2008 : Pharmacologically blocking PI3K significantly inhibited Akt and GSK3beta phosphorylation
Dal Col et al., Cell cycle (Georgetown, Tex.) 2008 (Lymphoma, Mantle-Cell) : Here we show that inhibition of PI3-K/Akt induces a 40 % decrease of cyclin D1 half-life as a result of accumulation of the dephosphorylated/active form of GSK-3beta within the nucleus, where this kinase can phosphorylate cyclin D1 on Thr286 thereby promoting its nuclear export
Yang et al., Proc Natl Acad Sci U S A 2009 : APC also induced phosphorylation of Ser-9 in glycogen synthase kinase 3beta ( GSK3beta ), which was blocked by the PI3K inhibitor LY294002
Uranga et al., Toxicological sciences : an official journal of the Society of Toxicology 2009 : Both Akt and GSK3beta phosphorylation were dependent on PI3K activation
Venkatesan et al., Cell Signal 2010 : Further, WISP1 stimulates PI3K-Akt dependent GSK3beta phosphorylation and beta-catenin nuclear translocation