CTNNB1 S33 mutants aren't phosphorylated by GSK3beta

Stable Identifier
Reaction [transition]
Homo sapiens
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S33 mutations of beta-catenin interfere with GSK3 phosphorylation and result in stabilization and nuclear localization of the protein and enhanced WNT signaling (Groen et al, 2008; Nhieu et al, 1999; Clements et al, 2002; reviewed in Polakis, 2000). S33 mutations have been identified in cancers of the central nervous system, liver, endometrium and stomach, 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
18757411 Illegitimate WNT pathway activation by beta-catenin mutation or autocrine stimulation in T-cell malignancies

Schilder-Tol, EJ, Spaargaren, M, Oud, ME, Overdijk, MB, Pals, ST, Groen, RW, Nusse, R, ten Berge, D

Cancer Res. 2008
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
Normal reaction
Functional status

Loss of function of pS37,T41,S45-CTNNB1 S33 mutants:Axin:GSK3:CK1alpha:APC:PP2A:AMER1 complex [cytosol]

Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
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