Siah-1 binds and regulates the function of Numb | Zendy

Laurent Susini | Zendy; Brent J. Passer | Zendy; Nathalie Amzallag-Elbaz | Zendy; Tamar JuvenGershon | Zendy; Sylvie Prieur | Zendy; Nicolas Privat | Zendy; Marcel Tuynder | Zendy; MarieClaude Gendron | Zendy; Alain Israël | Zendy; Robert Amson | Zendy; Moshe Oren | Zendy; Adam Telerman | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Siah-1 binds and regulates the function of Numb

Author(s) -

Laurent Susini,

Brent J. Passer,

Nathalie Amzallag-Elbaz,

Tamar JuvenGershon,

Sylvie Prieur,

Nicolas Privat,

Marcel Tuynder,

MarieClaude Gendron,

Alain Israël,

Robert Amson,

Moshe Oren,

Adam Telerman

Publication year - 2001

Publication title -

proceedings of the national academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.011

H-Index - 771

eISSN - 1091-6490

pISSN - 0027-8424

DOI - 10.1073/pnas.261571998

Subject(s) - numb , regulator , notch signaling pathway , microbiology and biotechnology , cell fate determination , biology , cytoplasm , transcription factor , genetics , gene , signal transduction

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 G(1) 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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research