Gene interactions and pathways from curated databases and text-mining

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CTNNB1 — LEF1

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

Orsulic et al., J Cell Sci 1999 : E-cadherin binding prevents beta-catenin nuclear localization and beta-catenin/LEF-1 mediated transactivation
Shtutman et al., Proc Natl Acad Sci U S A 1999 (Colonic Neoplasms) : Elevated beta-catenin levels in colorectal cancer caused by mutations in beta-catenin or by the adenomatous polyposis coli molecule, which regulates beta-catenin degradation, result in the binding of beta-catenin to LEF-1 and increased transcriptional activation of mostly unknown target genes
DasGupta et al., Development 1999 : In mice, TOPGAL expression was directly stimulated by a stabilized form of beta -catenin , but was also dependent upon LEF1/TCF3 in skin
Ben-Ze'ev et al., Ann N Y Acad Sci 1999 (Cell Transformation, Neoplastic) : Overexpression of wt plakoglobin or mutant beta-catenin lacking the transactivation domain induced nuclear accumulation of the endogenous beta-catenin and LEF-1-responsive transactivation
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
Kim et al., Cell Biol Int 2001 : Here, we investigated the effects of beta-catenin and LEF-1 on nuclear import of beta-catenin using different combinations of exogenous and endogenous molecules over longer lengths of time than previously studied
Filali et al., J Biol Chem 2002 : Wnt-3A/beta-catenin signaling induces transcription from the LEF-1 promoter
Kim et al., Cell Biol Int 2002 : beta-catenin has been shown to activate LEF-1 transcription during EMT induced in vitro by c-Fos ... In normal epithelial cell lines, such as HCE and MDCK cells, that contain functional APC, nuclear beta-catenin induced by exogenous LEF-1 is rapidly exported and EMT is not induced ... Our experiments demonstrated, however, that overexpressed LEF-1 upregulates nuclear beta-catenin and promotes dramatic EMT in DLD-1 epithelial tumors that retain nuclear beta-catenin ... Thus, our results demonstrate that LEF-1 can induce EMT directly when its transcription activity is activated by stable nuclear beta-catenin
Saito et al., Pigment Cell Res 2003 : The bHLH-LZ region of MITF-M is responsible for the physical interaction with LEF-1 , and beta-catenin is required for the collaboration between LEF-1 and MITF-M
Li et al., J Biol Chem 2004 : Furthermore, GRIP1 and beta-catenin can synergistically enhance the activity of both AR and Lef1 , and both coactivators are recruited specifically to AR-driven and Lef1-driven promoters
Toncheva et al., Tumour Biol 2004 (Colonic Neoplasms...) : Elevated beta-catenin levels in colorectal cancer result in the binding of beta-catenin to LEF-1 and increased transcriptional activation of the CCND1 gene
Sasaki et al., Dev Biol 2005 : LEF1 is a cell-type-specific transcription factor and mediates Wnt signaling pathway by association with its co-activator beta-catenin
Vadlamudi et al., J Cell Sci 2005 : Furthermore, beta-catenin in combination with PITX2 synergistically activates the LEF-1 promoter and this activation is independent of the Wnt-responsive element
Asally et al., Exp Cell Res 2005 : These findings indicate that beta-catenin alone can mediate the nuclear import of lef-1 through the direct binding
Ki et al., Cell Biol Int 2006 (Neoplasms) : Colon carcinoma cells containing an adenomatous polyposis coli mutation retain significant amounts of LEF-1 induced nuclear beta-catenin considerably after the time-point when beta-catenin disappears from the nuclei of LEF-1 transfected normal epithelial cells
Takeda et al., Nat Med 2006 (Adenoma...) : Mutant LEF1 not only inhibited expression of beta-catenin target genes but also stimulated expression of sebocyte markers, suggesting that it may determine the differentiated characteristics of sebaceous tumors
Xiong et al., Dev Cell 2006 : Mechanistically, Tob1a inhibits beta-catenin transcriptional activity by physically associating with beta-catenin and preventing the formation of beta-catenin/LEF1 complexes
Amen et al., Mol Cell Biol 2007 : PITX2 and beta-catenin interactions regulate Lef-1 isoform expression
Feigin et al., Cell Signal 2008 (Osteopetrosis) : OSTM1 regulates beta-catenin/Lef1 interaction and is required for Wnt/beta-catenin signaling
Varea et al., PloS one 2009 : The transcriptional activation of beta-catenin is dependent on lymphoid enhancer binding factor-1 ( LEF-1 ) and a truncated-mutant of LEF-1 almost completely blocks estradiol TCF mediated transcription
Novak et al., Proc Natl Acad Sci U S A 1998 (Cell Transformation, Neoplastic...) : We now show that modest overexpression of ILK in intestinal epithelial cells as well as in mammary epithelial cells results in an invasive phenotype concomitant with a down-regulation of E-cadherin expression, translocation of beta-catenin to the nucleus, formation of a complex between beta-catenin and the high mobility group transcription factor, LEF-1, and transcriptional activation by this LEF-1/beta-catenin complex
Simcha et al., J Cell Biol 1998 : Overexpression of wild-type plakoglobin or mutant beta-catenin lacking the transactivation domain induced accumulation of the endogenous beta-catenin in the nucleus and LEF-1-responsive transactivation