Gene interactions and pathways from curated databases and text-mining

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AXIN1 — CTNNB1

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 *

Text-mined interactions from Literome

Kishida et al., Oncogene 1999 : Axin prevents Wnt-3a induced accumulation of beta-catenin
Yamamoto et al., J Biol Chem 1999 : Axin forms a complex with glycogen synthase kinase-3beta ( GSK-3beta ) and beta-catenin and promotes GSK-3beta dependent phosphorylation of beta-catenin , thereby stimulating the degradation of beta-catenin
Kishida et al., Mol Cell Biol 1999 : Although expression of Axin in SW480 cells caused the degradation of beta-catenin and reduced the cell growth rate, expression of an Axin mutant that lacks the DIX domain did not affect the level of beta-catenin or the growth rate
Thomas et al., FEBS Lett 1999 : The Axin dependent phosphorylation of beta-catenin catalysed by glycogen synthase kinase-3 ( GSK3 ) is inhibited during embryogenesis
Kodama et al., J Biol Chem 1999 : Axin , a Wnt signal negative regulator, enhances glycogen synthase kinase (GSK)-3beta dependent phosphorylation of beta-catenin and stimulates the degradation of beta-catenin ... These results suggest that Axin regulates the stability of plakoglobin by enhancing its phosphorylation by GSK-3beta and that Axin may act on beta-catenin and plakoglobin in similar manners
Kawahara et al., J Biol Chem 2000 : Down-regulation of beta-catenin by the colorectal tumor suppressor APC requires association with Axin and beta-catenin ... In the present study, we examined whether APC association with Axin is required for degradation of beta-catenin
Spink et al., EMBO J 2000 : In the absence of Wnt signal, Axin and APC regulate cytoplasmic levels of the proto-oncogene beta-catenin through the formation of a large complex containing these three proteins, glycogen synthase kinase 3beta ( GSK3beta ) and several other proteins
von Kries et al., Nat Struct Biol 2000 : Interactions between beta-catenin and LEF-1/TCF, APC and conductin/axin are essential for wnt controlled stabilization of beta-catenin and transcriptional activation ... Moreover, we demonstrate that conductin/axin binding to beta-catenin is essential for beta-catenin degradation, and that APC acts as a cofactor of conductin/axin in this process
Bax et al., Structure 2001 : This inhibits the Axin dependent phosphorylation of beta-catenin by GSK-3
Amit et al., Genes Dev 2002 : Axin mediated CKI phosphorylation of beta-catenin at Ser 45 : a molecular switch for the Wnt pathway
Kusano et al., Mol Cell Biol 2002 : This interaction inhibited Axin mediated downregulation of free levels of cytosolic beta-catenin
Cong et al., Proc Natl Acad Sci U S A 2004 : Nuclear-cytoplasmic shuttling of Axin regulates subcellular localization of beta-catenin
Ruiz et al., Dev Dyn 2004 : Biochemical analysis revealed that such an increase in betacatenin was due to the disruption of Axin/GSK3beta/betacatenin complexes promoted by the increased expression of Frat, the mouse homologue of GSK3betabinding protein ( GBP ), in epidermis, precluding the degradation of betacatenin
Hirabayashi et al., J Neurochem 2004 : Thereby, S-SCAM inhibited the Axin mediated phosphorylation of beta-catenin by GSK3beta
Liu et al., Curr Biol 2005 : In the `` canonical '' Wnt signaling pathway, Disheveled ( Dvl ) is required to functionally inhibit the activity of the GSK3beta/Axin complex and thereby stabilize beta-catenin ... We conclude that rapid disruption of GSK3beta/Axin interactions in response to Wnt leads to the initial stabilization of beta-catenin and that Galpha ( o ) and Galpha ( q ) signaling contributes to Wnt mediated GSK3beta/Axin disruption and the ultimate stabilization of beta-catenin
Carayol et al., Cell Signal 2006 : Here we report that IKKalpha could inhibit beta-catenin degradation mediated not only by the Axin/APC/GSK-3beta complex, but also by the Siah-1 pathway
Yang et al., J Biol Chem 2006 (Adenomatous Polyposis Coli...) : APC binds beta-catenin and is involved in the Axin complex, suggesting that APC regulates beta-catenin phosphorylation
Kofron et al., Development 2007 : Wnt11/beta-catenin signaling in both oocytes and early embryos acts through LRP6 mediated regulation of axin
Kikuchi et al., Cancer Sci 2008 (Neoplasms) : The significance of Wnt signaling in human cancer has been elucidated by the identification of mutations in genes coding for the beta-catenin dependent pathway components, adenomatous polyposis coli gene product, beta-catenin, and Axin
Haÿ et al., Mol Cell Biol 2009 : These data indicate that a previously unrecognized N-cadherin-axin-LRP5 interaction negatively regulates Wnt/beta-catenin signaling and is critical in the regulation of osteoblast function, bone formation, and bone mass
Salisbury et al., Mol Endocrinol 2009 : Overexpression of AXIN , an inhibitor of beta-catenin , also reduces GnRH stimulation of TOPflash
Wu et al., PloS one 2009 : In this study, we reconstituted Axin dependent beta-catenin phosphorylation by GSK3 and CK1 in vitro using recombinant proteins, and found that the phosphorylated PPPSPXS peptides directly inhibit beta-catenin phosphorylation by GSK3 in a sequence and phosphorylation dependent manner
Qu et al., Nat Cell Biol 2010 : Wnt7a and active beta-catenin promote neural stem cell self-renewal, whereas the deletion of Wnt7a or the lentiviral transduction of axin , a beta-catenin inhibitor , led to decreased cell proliferation in adult neurogenic areas
Sakanaka et al., Proc Natl Acad Sci U S A 1998 : In mammalian cells, Axin inhibits Wnt-1 stimulation of beta-catenin/lymphoid enhancer factor 1-dependent transcription
Kishida et al., J Biol Chem 1998 : Furthermore, Axin stimulated the degradation of beta-catenin in COS cells ... Taken together with our recent observations that Axin directly interacts with glycogen synthase kinase-3beta ( GSK-3beta ) and beta-catenin and that it promotes GSK-3beta dependent phosphorylation of beta-catenin , these results suggest that Axin, APC, GSK-3beta, and beta-catenin make a tetrameric complex, resulting in the regulation of the stabilization of beta-catenin
Hart et al., Curr Biol 1998 (Adenomatous Polyposis Coli) : Overexpression of hAxin strongly promoted the downregulation of wild-type beta-catenin in colon cancer cells, whereas mutant oncogenic beta-catenin was unaffected