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GSK3B — ILK

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: GSK3B → Complex of ILK-LIMS1-PARVA-PXN (increases)
  Attwell et al., Mol Biol Cell 2003*
  Evidence: # Ariadne: Furthermore, CH-ILKBP stimulated GSK-3 beta phosphorylation on Ser 9, and phosphorylation of PKB/Akt on Ser 473, both of which have been shown previously to be regulated by ILK (Delcommenne et al., 1998 ). [Regulation]
• OpenBEL Selventa BEL large corpus: GSK3B → ILK (increases, GSK3B Activity) Attwell et al., Mol Biol Cell 2003*
  Evidence: # Ariadne: Furthermore, CH-ILKBP stimulated GSK-3 beta phosphorylation on Ser 9, and phosphorylation of PKB/Akt on Ser 473, both of which have been shown previously to be regulated by ILK (Delcommenne et al., 1998 ). [Regulation]

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Ophid Interaction: ILK — GSK3B (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Leung-Hagesteijn et al., EMBO J 2001 : Catalytically active, but not mutant ILKAP, strongly inhibited insulin-like growth factor-1 stimulated GSK3beta phosphorylation on Ser9, but did not affect phosphorylation of PKB on Ser473, suggesting that ILKAP selectively affects ILK mediated GSK3beta signalling
Miller et al., Biochem Biophys Res Commun 2003 : Inhibition of GSK3beta by LiCl blocks L6 myogenesis, indicating that ILK mediated inhibition of GSK3beta is not sufficient for differentiation
Kumar et al., Oncogene 2004 (Cell Transformation, Neoplastic) : Consistent with the silencing data, ILKAP inhibition of ILK selectively inhibited S9 phosphorylation of GSK3beta without affecting S473 phosphorylation of PKB
Rosanò et al., Cancer Res 2005 (Neoplasm Invasiveness...) : 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, activity, and invasiveness, indicating that ET-1/ET ( A ) R-induced EMT promoting effects depend on ILK
Tamura et al., Cancer Sci 2006 (Cell Transformation, Neoplastic) : PP2Cdelta/ILKAP also forms a complex with ILK1 to inhibit the GSK3beta mediated integrin-ILK1 signaling in vivo, inhibiting cell cycle progression
Naska et al., J Neurosci 2006 : In sympathetic neurons, ILK phosphorylated and inhibited GSK-3beta , and inhibition of GSK-3beta ( either pharmacologically, with dominant negative GSK-3beta, or by genetic knockdown ) caused robust dendrite initiation
Joshi et al., FASEB J 2007 : Integrin linked kinase (ILK) , a membrane proximal upstream regulator of Akt and GSK3beta , was considered a candidate signaling mediator for T-cad
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
Medici et al., Matrix Biol 2010 : ILK also causes inhibitory phosphorylation of GSK-3beta , a kinase that prevents functional activation of both Snail and LEF-1
Huang et al., Microcirculation 2010 (Mechanotransduction, Cellular) : ILK was localized to FA and silencing ILK promoted cell spreading, enhanced cell adhesion, reduced cell proliferation and reduced downstream phosphorylation of GSK-3beta and PKB/Akt