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

doi:10.1073/pnas.261571998

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 journal › Article › peer-review

86 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 language	English
Pages (from-to)	15067-15072
Number of pages	6
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	98
Issue number	26
DOIs	https://doi.org/10.1073/pnas.261571998
State	Published - 18 Dec 2001
Externally published	Yes

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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.",

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AU - Susini, Laurent

AU - Passer, Brent J.

AU - Amzallag-Elbaz, Nathalie

AU - Juven-Gershon, Tamar

AU - Prieur, Sylvie

AU - Privat, Nicolas

AU - Tuynder, Marcel

AU - Gendron, Marie Claude

AU - Israël, Alain

AU - Amson, Robert

AU - Oren, Moshe

AU - Telerman, Adam

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AB - 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.

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Siah-1 binds and regulates the function of Numb

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