◀ Back to CTNNB1

CTNNB1 — IGF1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CTNNB1 → IGF1 (increases, IGF1 Activity) Playford et al., Proc Natl Acad Sci U S A 2000*
  Evidence: To investigate whether IGF-1 also enhanced transactivation potential, a reporter gene assay was performed in HEK293 cells. We used a reporter construct incorporating multimeric Lef/Tcf promoter sequences upstream of a luciferase reporter (TOPFLASH) and a control construct containing mutated promoter sequences (FOPFLASH, ref. 21). We cotransfected TOPFLASH or FOPFLASH, ?-catenin, and human wild-type Tcf-4 wild-type expression constructs into 293 cells. Optimized luciferase assays showed a basal l...
• OpenBEL Selventa BEL large corpus: CTNNB1 → IGF1 (increases) Playford et al., Proc Natl Acad Sci U S A 2000*
  Evidence: We found that IGF-1 stimulation enhanced tyrosine phosphorylation of two proteins, beta-catenin and insulin-receptor substrate 1, which formed a complex with E-cadherin. Tyrosine phosphorylation of beta-catenin was accompanied by rapid (<1 min) dissociation from E-cadherin at the plasma membrane, followed by relocation to the cellular cytoplasm.
• NCI Pathway Database Stabilization and expansion of the E-cadherin adherens junction: IGF1 (IGF1) → E-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1-CTNNA1-CTNND1) (modification, collaborate)
  Qian et al., EMBO J 2004
  Evidence: assay, physical interaction

Text-mined interactions from Literome

Playford et al., Proc Natl Acad Sci U S A 2000 (Colorectal Neoplasms) : Insulin-like growth factor 1 regulates the location, stability, and transcriptional activity of beta-catenin ... In conclusion, we have shown that IGF-1 causes tyrosine phosphorylation and stabilization of beta-catenin
Desbois-Mouthon et al., Oncogene 2001 (Carcinoma, Hepatocellular) : Together with inhibiting GSK-3beta, insulin and IGF-1 increased the cytoplasmic levels of beta-catenin
Satyamoorthy et al., Cancer Res 2001 (Disease Progression...) : IGF-1 also activated Akt, inhibited its down-stream effector GSK3-beta, and stabilized beta-catenin
Kuemmerle et al., Am J Physiol Gastrointest Liver Physiol 2005 : Endogenous IGF-I inhibited beta-catenin phosphorylation, caspase 3 activation, and apoptosis induced by serum deprivation
Verras et al., Mol Endocrinol 2005 (Prostatic Neoplasms) : It has been shown that IGF-I increases the cellular level of beta-catenin , an AR coactivator ... Moreover, using a pulse-chase experiment, we showed that IGF-I enhances the stability of beta-catenin in prostate cancer cells
Chen et al., J Biol Chem 2005 : Functional significance of type 1 insulin-like growth factor mediated nuclear translocation of the insulin receptor substrate-1 and beta-catenin ... IRS-1 is required for IGF-1 mediated nuclear translocation of beta-catenin , resulting in the activation of the beta-catenin target genes ... IGF-1 mediated nuclear translocation of beta-catenin is facilitated by the nuclear translocation of IRS-1
Shanely et al., Am J Physiol Cell Physiol 2009 : Finally, IGF-I increased nuclear beta-catenin protein, and small interfering RNA knockdown of beta-catenin attenuated IGF-I induced 1.3-kb type IIb MyHC promoter activity and type IIb MyHC mRNA
Wang et al., J Bone Miner Res 2010 : The results show that IGF-1 and the IGF- receptor (IGF1R) stimulate Wnt-4 expression and beta-catenin activation in growth plate chondrocytes
Ye et al., Glia 2010 : Inhibiting the PI3-Akt pathway suppressed IGF-I induced increases in beta-catenin and cyclin D1 mRNA, while suppression of GSK3beta activity simulated IGF-I actions