Gene interactions and pathways from curated databases and text-mining

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GSK3B — TCF21

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