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GSK3B — TCF23
Text-mined interactions from Literome
Staal et al., Int Immunol 1999
:
That is, a dominant negative
GSK-3beta does not specifically activate Tcf transcription and stimuli ( lithium or phytohemagglutinin ) that inhibit GSK-3beta activity also do not
activate Tcf reporter genes
Chen et al., Proc Natl Acad Sci U S A 2001
:
Dvl proteins participate as key intermediates in signal transmission from the seven membrane spanning Frizzled receptors leading to inhibition of glycogen synthase kinase-3beta (
GSK-3beta ), stabilization of beta-catenin, and
activation of the lymphoid enhancer factor ( LEF )
transcription factor
Ciani et al., J Cell Biol 2004
:
Inhibition of
GSK-3beta by DVL
increases beta-catenin stability and
TCF transcriptional activation
Smith et al., J Biol Chem 2005
:
Glucocorticoids inhibit the transcriptional activity of
LEF/TCF in differentiating osteoblasts in a
glycogen synthase kinase-3beta dependent and -independent manner
Erdal et al., Int J Cancer 2005
(Carcinoma, Hepatocellular) :
Lithium
induced the accumulation of N-terminally phosphorylated inactive form of
GSK3beta with concomitant increase in beta-catenin and
beta-catenin/TCF transcriptional activity in both cell lines
Xu et al., Cell Death Differ 2007
(Alzheimer Disease) :
Intracellular domains of amyloid precursor-like protein 2 interact with CP2
transcription factor in the nucleus and
induce glycogen synthase kinase-3beta expression ... In this study, we demonstrate that the APLP2-ICDs interact with CP2/LSF/LBP1 ( CP2 )
transcription factor in the nucleus and
induce the expression of
glycogen synthase kinase 3beta ( GSK-3beta ), which has broad ranged substrates such as tau- and beta-catenin ... Taken together, these results suggest that APLP2-ICDs contribute to the AD pathogenesis, by
inducing GSK-3beta expression through the interaction with CP2
transcription factor in the nucleus
Salins et al., Neurosci Lett 2007
(Neuroblastoma) :
This was accompanied by reduction in active
GSK-3beta , and
increased nuclear translocation of beta-catenin,
TCF-3 , and LEF-1
Lim et al., Cancer Res 2008
(Bile Duct Neoplasms...) :
The
GSK-3beta inhibitor, SB216763, partially
prevented DHA induced reduction of beta-catenin protein and
TCF/LEF reporter activity, and restored cell growth, suggesting the involvement of GSK-3beta dephosphorylation in omega 3-PUFA induced beta-catenin degradation