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CTNNB1 — ILK

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CTNNB1 → ILK (increases, ILK Activity, CTNNB1 Activity) Oloumi et al., Oncogene 2006*
  Evidence: We now report that molecular and pharmacological inhibition of ILK activity in mammalian cells directly modulates Wnt signaling by suppressing the stabilization and nuclear translocation of beta-catenin, as well as beta-catenin/Lef-mediated transcription. I
• NCI Pathway Database Integrin-linked kinase signaling: beta catenin (CTNNB1) → ILK (ILK) (modification, collaborate) Shtutman et al., Proc Natl Acad Sci U S A 1999*, Novak et al., Proc Natl Acad Sci U S A 1998*
  Evidence: physical interaction

Text-mined interactions from Literome

Wu et al., J Cell Sci 1999 : Furthermore, ILK regulates nuclear translocation of ( beta)-catenin and gene expression, and promotes cell cycle progression and tumor formation
Yoganathan et al., Biochem Pharmacol 2000 : We have shown that ILK overexpression results in the translocation of beta-catenin to the nucleus, which then forms a complex formation with the lymphoid enhancer binding factor 1 ( LEF-1 ) transcription factor, subsequently activating the transcriptional activity of promoters containing LEF-1 response elements
Tan et al., Oncogene 2001 (Adenomatous Polyposis Coli...) : Inhibition of ILK resulted in decreased nuclear beta-catenin expression, and in the inhibition of phosphorylation of GSK-3 and stimulation of its activity, leading to accelerated degradation of beta-catenin ... These data demonstrate that ILK can regulate beta-catenin/TCF and snail transcription factors by distinct pathways
Persad et al., J Cell Biol 2001 : We define a pathway that involves mainly integrin linked kinase and glycogen synthase kinase 3 in the PTEN dependent regulation of beta-catenin stability, nuclear beta-catenin expression, and transcriptional activity
Oloumi et al., Biochim Biophys Acta 2004 : More specifically, pathological overexpression of ILK results in down-regulation of E-cadherin expression, and nuclear accumulation of beta-catenin, leading to the subsequent activation of the beta-catenin/Tcf transcription complex, the downstream components of the Wnt signalling pathway
Iwano et al., Curr Opin Nephrol Hypertens 2004 (Fibrosis...) : The intracellular signaling pathways leading to initiation of epithelial-mesenchymal transition remain largely unknown, though recent studies have identified beta-catenin and Smad3 activation of lymphoid enhancer factor, integrin linked kinase , and small GTPases and mitogen activated protein kinases as key components
Douglas et al., Am J Respir Cell Mol Biol 2006 (Necrosis...) : Reduced E-cadherin expression after 6 d of BHT and hyperoxia was accompanied by enhanced expression and nuclear localization of beta-catenin and increased integrin linked kinase-1 expression during subsequent normoxic recovery
Oloumi et al., Oncogene 2006 : Modulation of Wnt3a mediated nuclear beta-catenin accumulation and activation by integrin linked kinase in mammalian cells
Joshi et al., FASEB J 2007 : Furthermore, ILK-GSK3beta dependent modulation of active beta-catenin levels by GPI anchored T-cad represents a novel mechanism for controlling cellular beta-catenin activity
Bagnato et al., Cells Tissues Organs 2007 (Disease Progression...) : Transfection of dominant negative ILK or exposure to an ILK inhibitor suppresses the ET-1 induced phosphorylation of GSK-3beta as well as Snail and beta-catenin protein stability, transcriptional activity and invasiveness, indicating that ET-1/ET ( A ) R-induced EMT depends on ILK activity
Dwivedi et al., Basic Res Cardiol 2008 (Carotid Artery Injuries...) : Regulation of cell-matrix contacts and beta-catenin signaling in VSMC by integrin linked kinase : implications for intimal thickening
Nie et al., J Biol Chem 2009 : The activity of integrin linked kinase was required for the effect of SPARC on beta-catenin accumulation as well as extracellular matrix remodeling
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
Delcommenne et al., Proc Natl Acad Sci U S A 1998 : In addition, ILK induces nuclear translocation of beta-catenin , where the latter associates with a T cell factor/lymphocyte enhancer binding factor 1 ( TCF/LEF-1 ) to form an activated transcription factor