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CTNNB1 — PIK3R1
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
CTNNB1
—
PIK3R1
(direct interaction, pull down)
Espada et al., J Cell Biol 1999*
-
IRef Hprd Interaction:
CTNNB1
—
PIK3R1
(in vitro)
Espada et al., J Cell Biol 1999*, Woodfield et al., Biochem J 2001*
-
IRef Hprd Interaction:
CTNNB1
—
PIK3R1
(in vivo)
Espada et al., J Cell Biol 1999*, Woodfield et al., Biochem J 2001*
-
IRef Innatedb Interaction:
Complex of CTNNA1-CTNNB1-PIK3R1-CTNNB1-CTNNA1-PIK3R1
(unknown, -)
Vogelmann et al., J Cell Sci 2005*
-
IRef Ophid Interaction:
CTNNB1
—
PIK3R1
(aggregation, confirmational text mining)
Woodfield et al., Biochem J 2001*
-
IRef Ophid Interaction:
CTNNB1
—
PIK3R1
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Sharma et al., J Biol Chem 2002
(Prostatic Neoplasms) :
Phosphatidylinositol 3-kinase/Akt stimulates androgen pathway through GSK3beta inhibition and nuclear
beta-catenin accumulation
Morrison et al., J Virol 2003
:
The cytoplasmic accumulation of
beta-catenin downstream of LMP2A was
independent of
PI3K signaling, whereas its nuclear translocation was dependent on PI3K signaling
Everly et al., J Virol 2004
:
Activation of
PI3K can
affect the activity of
beta-catenin , the target of the wnt signaling pathway ... Neither the cytoplasmic accumulation of
beta-catenin nor the nuclear inactivation of GSK3beta was
affected by the inhibition of
PI3K signaling
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
Chung et al., J Endocrinol 2008
:
Our data also suggest that
PI3K/Akt mediated inactivation of GSK-3beta and stabilization of
beta-catenin contribute to the anti-apoptotic effects of ghrelin
Xia et al., Mol Cell Biol 2010
:
Interestingly, the activation of PI3K/Akt appeared to be independent of the activation of PKA, whereas both
PI3K/Akt and PKA signaling inactivated GSK-3 and
increased beta-catenin translocation
Sonderegger et al., Endocrinology 2010
:
Chemical inhibition of
PI3K abolished Wnt dependent phosphorylation of AKT and GSK-3beta and trophoblast motility but did not
affect appearance of activated
beta-catenin or Wnt/TCF reporter activity
Venkatesan et al., Cell Signal 2010
:
Further, WISP1 stimulates
PI3K-Akt dependent GSK3beta phosphorylation and
beta-catenin nuclear translocation
Lee et al., Bone 2010
:
Role of
PI3K on the regulation of BMP2 induced
beta-Catenin activation in human bone marrow stem cells ... In addition, BMP2 induced
beta-Catenin activity and ALP activity were
blocked by
PI3K inhibition
Wang et al., J Bone Miner Res 2010
:
T ( 3 ) -mediated Wnt-4 expression,
beta-catenin activation, cell proliferation, and terminal differentiation of growth plate chondrocytes are partially
prevented by the IGF1R inhibitor picropodophyllin as well as by the
PI3K/Akt signaling inhibitors LY294002 and Akti1/2
Lee et al., Gastroenterology 2010
(Colitis...) :
PI3K inhibition in interleukin-10 ( -/- ) mice
impaired colitis induced epithelial Akt and
beta-catenin activation, reduced progenitor cell expansion, and prevented dysplasia ... Biochemical analyses indicated that
PI3K-Akt signaling
increased nuclear total beta-catenin and
P-beta-catenin ( 552 ) levels and reduced N-terminal beta-catenin phosphorylation, which is associated with degradation ...
PI3K induced and Akt mediated
beta-catenin signaling are required for progenitor cell activation during the progression from CUC to CAC ; these factors might be used as biomarkers of dysplastic transformation in the colon