◀ Back to CTNNB1
CTNNB1 — IGF1
Pathways - manually collected, often from reviews:
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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...
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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.
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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