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A more recent version of this article appeared on January 6, 2006
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M509060200v1
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Papers In Press, published online ahead of print October 17, 2005
J. Biol. Chem, 10.1074/jbc.M509060200
Submitted on August 17, 2005
Revised on October 17, 2005
Accepted on October 17, 2005

SIAH1 interacts with the scaffold protein posh to promote JNK activation and apoptosis

Zhiheng Xu, Andrew Sproul, Wenyi Wang, Nikolay Kukekov, and Lloyd Greene

Department of Pathology, Columbia University College of Physicians and Surgeons, New York, NY 10032

Corresponding Author: zhxu{at}genetics.ac.cn

Siah proteins are E3 ubiquitin ligases that have been implicated in a variety of cellular actions including promotion of apoptotic death. Here, we show that Siah1 is a binding partner for POSH (plenty of SH3’s), a scaffold component of the apoptotic JNK pathway, and that Siah contributes to death of neurons and other cell types by activating the JNK pathway. Such pro-apoptotic activity requires Siah1’s E3 ligase activity. Moreover, apoptotic stimuli markedly elevate cellular Siah1 levels by a mechanism reliant on Siah1 protein stabilization. This stabilization requires JNK pathway activation and interaction with POSH, and is enhanced by phosphorylation of SIAH1 at tyrosines 100 and 126. Depletion of intracellular Siah proteins via siRNA partially protects cells from death evoked by apoptotic stimuli such as trophic factor deprivation and DNA damage. These findings thus reveal a “loop” mechanism in which the JNK pathway promotes SIAH1 stabilization and in which SIAH1 in turn activates the JNK pathway and, ultimately, contributes to cell death.


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