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

Ersheng Kuang, Qingwen Wan, Xiaojuan Li, Hua Xu, Tingting Zou, Yipeng Qi

Research output: Contribution to journalArticle

42 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1983-1988
Number of pages6
JournalExperimental Cell Research
Volume312
Issue number11
DOIs
StatePublished - Jul 1 2006

Keywords

  • Apoptosis
  • ER Ca depletion
  • ER stress
  • Endoplasmic-reticulum-specific pathways
  • Nogo-B/ASY

ASJC Scopus subject areas

  • Cell Biology

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