CTNNB1 S37 mutants aren't phosphorylated by GSK3beta

Stable Identifier
R-HSA-4839635
Type
Reaction [transition]
Species
Homo sapiens
Compartment
cytosol
ReviewStatus
5/5
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CTNNB1 S37 mutants aren't phosphorylated by GSK3beta
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S37 mutations of beta-catenin interfere with GSK3 phosphorylation and stabilize the protein, resulting in enhanced WNT pathway signaling (Nhieu et al, 1999; Clements et al, 2002; reviewed in Polakis, 2000). S37 mutations have been identified in cancers of the brain, liver, ovary and large intestine, among others (reviewed in Polakis, 2000).
Literature References
PubMed ID Title Journal Year
10487827 Nuclear accumulation of mutated beta-catenin in hepatocellular carcinoma is associated with increased cell proliferation

Zafrani, ES, Renard, CA, Wei, Y, Cherqui, D, Nhieu, JT, Buendia, MA

Am. J. Pathol. 1999
10921899 Wnt signaling and cancer

Polakis, P

Genes Dev. 2000
12067995 beta-Catenin mutation is a frequent cause of Wnt pathway activation in gastric cancer

Sarnaik, A, Wang, J, Lowy, AM, MacDonald, J, Kim, OJ, Fenoglio-Preiser, C, Groden, J, Clements, WM

Cancer Res. 2002
Participants
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as an event of
Normal reaction
Phosphorylation of phospho- (Ser45, Thr41) beta-catenin at Ser37 by GSK-3 (Homo sapiens)
Functional status

Loss of function of pT41,S45-CTNNB1 S37 mutants:Axin:GSK3:CK1alpha:APC:PP2A:AMER1 complex [cytosol]

Normal Entity
Disease Entity
Status
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Authored
Rothfels, K  (2013-10-30)
Reviewed
Salahshor, S  (2014-05-12)
Woodgett, J  (2014-05-22)
Created
Rothfels, K  (2013-11-01)
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