RGD Reference Report - Control of beta-catenin phosphorylation/degradation by a dual-kinase mechanism. - Rat Genome Database

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Control of beta-catenin phosphorylation/degradation by a dual-kinase mechanism.

Authors: Liu, C  Li, Y  Semenov, M  Han, C  Baeg, GH  Tan, Y  Zhang, Z  Lin, X  He, X 
Citation: Liu C, etal., Cell. 2002 Mar 22;108(6):837-47.
RGD ID: 10449517
Pubmed: PMID:11955436   (View Abstract at PubMed)

Wnt regulation of beta-catenin degradation is essential for development and carcinogenesis. beta-catenin degradation is initiated upon amino-terminal serine/threonine phosphorylation, which is believed to be performed by glycogen synthase kinase-3 (GSK-3) in complex with tumor suppressor proteins Axin and adnomatous polyposis coli (APC). Here we describe another Axin-associated kinase, whose phosphorylation of beta-catenin precedes and is required for subsequent GSK-3 phosphorylation of beta-catenin. This "priming" kinase is casein kinase Ialpha (CKIalpha). Depletion of CKIalpha inhibits beta-catenin phosphorylation and degradation and causes abnormal embryogenesis associated with excessive Wnt/beta-catenin signaling. Our study uncovers distinct roles and steps of beta-catenin phosphorylation, identifies CKIalpha as a component in Wnt/beta-catenin signaling, and has implications to pathogenesis/therapeutics of human cancers and diabetes.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of canonical Wnt signaling pathway involved_inICGO:001810510449517PMID:11955436ParkinsonsUK-UCL 

Molecular Function
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
protein serine/threonine kinase activity enablesIDA 10449517PMID:11955436ParkinsonsUK-UCL 

Objects Annotated

Genes (Rattus norvegicus)
Csnk1a1  (casein kinase 1, alpha 1)


Additional Information