Abstract
The expanded polyglutamine (polyQ) tracts observed in autosomal dominant neurodegenerative disorders have the tendency to form intracellular aggregates, thus enhancing apoptotic cell death and the formation of autophagic vesicles. PolyQ accumulation inhibits the ERassociated degradation system (ERAD) resulting in reduced retrotranslocation from the ER and increased accumulation of misfolded proteins in the lumen of ER. Autophagy is an early cellular defense mechanism associated with ER stress, but prolonged ER stress may induce autophagic cell death, with destruction of cellular components and apoptotic cell death. Endoplasmic reticulum (ER) stress may be the key signal for both of these events.
Keywords: microtubles, proapoptotic Bcl-2 family, Caspase-12, polyQ aggregation, preautophagosomal membrane
Current Molecular Medicine
Title: Conformational Diseases and ER Stress-Mediated Cell Death: Apoptotic Cell Death and Autophagic Cell Death
Volume: 6 Issue: 1
Author(s): Takashi Momoi
Affiliation:
Keywords: microtubles, proapoptotic Bcl-2 family, Caspase-12, polyQ aggregation, preautophagosomal membrane
Abstract: The expanded polyglutamine (polyQ) tracts observed in autosomal dominant neurodegenerative disorders have the tendency to form intracellular aggregates, thus enhancing apoptotic cell death and the formation of autophagic vesicles. PolyQ accumulation inhibits the ERassociated degradation system (ERAD) resulting in reduced retrotranslocation from the ER and increased accumulation of misfolded proteins in the lumen of ER. Autophagy is an early cellular defense mechanism associated with ER stress, but prolonged ER stress may induce autophagic cell death, with destruction of cellular components and apoptotic cell death. Endoplasmic reticulum (ER) stress may be the key signal for both of these events.
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Cite this article as:
Momoi Takashi, Conformational Diseases and ER Stress-Mediated Cell Death: Apoptotic Cell Death and Autophagic Cell Death, Current Molecular Medicine 2006; 6 (1) . https://dx.doi.org/10.2174/156652406775574596
DOI https://dx.doi.org/10.2174/156652406775574596 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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