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

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.

journal_name

Exp Cell Res

authors

Kuang E,Wan Q,Li X,Xu H,Zou T,Qi Y

doi

10.1016/j.yexcr.2006.02.024

subject

Has Abstract

pub_date

2006-07-01 00:00:00

pages

1983-8

issue

11

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(06)00084-X

journal_volume

312

pub_type

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