◀ Back to PIK3R1
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