Siah-1 binds and regulates the function of Numb

Laurent Susini, Brent J. Passer, Nathalie Amzallag-Elbaz, Tamar Juven-Gershon, Sylvie Prieur, Nicolas Privat, Marcel Tuynder, Marie Claude Gendron, Alain Israël, Robert Amson, Moshe Oren, Adam Telerman

Research output: Contribution to journalArticlepeer-review

85 Scopus citations

Abstract

The Drosophila Seven in absentia (Sina) gene product originally was described as a protein that controls cell fate decisions during eye development. Its mammalian homolog, Siah-1, recently was found to be involved in p53-dependent and -independent pathways of apoptosis and G1 arrest. We report that Siah-1 interacts directly with and promotes the degradation of the cell fate regulator Numb. Siah-1-mediated Numb degradation leads to redistribution of endogenous cell-surface Notch to the cytoplasm and nucleus and to augmented Notch-regulated transcriptional activity. These data imply that through its ability to target Numb for degradation, Siah-1 can act as a key regulator of Numb-related activities, including Notch signaling.

Original languageEnglish
Pages (from-to)15067-15072
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume98
Issue number26
DOIs
StatePublished - 18 Dec 2001
Externally publishedYes

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