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Exp Cell Res. 2006 Jul 1;312(11):1983-8. Epub 2006 May 9.

ER stress triggers apoptosis induced by Nogo-B/ASY overexpression.

Author information

1
State Key Laboratory of Virology, Section of Molecular Virology, College of Life Science, Wuhan University, Wuhan 430072, PR China.

Abstract

Nogo-B/ASY has been characterized as a novel human apoptosis-inducing protein without any known apoptosis-related motifs. However, the validity of Nogo-B/ASY as a physiological apoptotic protein was recently questioned. In present research, we demonstrate that ASY overexpression contributes to ER stress and induces apoptosis through ER Ca2+ depletion and ER-specific pathways. ER stress and the disorder of intracellular calcium trigger the apoptosis induced by ASY overexpression. At the same time, stable transfectants overexpressing high levels of ASY are resistant to ER-stress-associated stimuli, which implies that ASY overexpression activates protective response in response to ER stress. Our results provide a direct apoptotic pathway that ASY overexpression induces apoptosis through ER stress and ER-specific signal pathways.

PMID:
16687140
DOI:
10.1016/j.yexcr.2006.02.024
[Indexed for MEDLINE]

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