Our hosting provider is investigating network issues. We apologize for the inconvenience.

Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Siah-1 mediates a novel beta-catenin degradation pathway linking p53 to the adenomatous polyposis coli protein.

Molecular cell | May 6, 2001

The adenomatous polyposis coli (APC) tumor-suppressor protein, together with Axin and GSK3beta, forms a Wnt-regulated signaling complex that mediates phosphorylation-dependent degradation of beta-catenin by the proteasome. Siah-1, the human homolog of Drosophila seven in absentia, is a p53-inducible mediator of cell cycle arrest, tumor suppression, and apoptosis. We have now found that Siah-1 interacts with the carboxyl terminus of APC and promotes degradation of beta-catenin in mammalian cells. The ability of Siah-1 to downregulate beta-catenin signaling was also demonstrated by hypodorsalization of Xenopus embryos. Unexpectedly, degradation of beta-catenin by Siah-1 was independent of GSK3beta-mediated phosphorylation and did not require the F box protein beta-TrCP. These results indicate that APC and Siah-1 mediate a novel beta-catenin degradation pathway linking p53 activation to cell cycle control.

Pubmed ID: 11389840 RIS Download

Mesh terms: Adenomatous Polyposis Coli Protein | Animals | Calcium-Calmodulin-Dependent Protein Kinases | Cell Cycle | Cytoskeletal Proteins | Embryo, Mammalian | Embryo, Nonmammalian | GTP-Binding Proteins | Glycogen Synthase Kinase 3 | Humans | Neoplasm Proteins | Nuclear Proteins | Phosphorylation | Protein Binding | Signal Transduction | Trans-Activators | Tumor Cells, Cultured | Tumor Suppressor Protein p53 | Ubiquitin-Protein Ligases | Xenopus | Xenopus Proteins | beta Catenin | beta-Transducin Repeat-Containing Proteins

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.