Journal
GENES & DEVELOPMENT
Volume 23, Issue 19, Pages 2253-2259Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1858009
Keywords
Amyotrophic lateral sclerosis; unfolded protein response; endoplasmic reticulum stress; XBP-1; autophagy
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Funding
- Agence Nationale pour la Recherche
- European Union
- Austrian Science Fund (FWF) [S-9304-B05]
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Cellular defense mechanisms, including the unfolded protein response (UPR) and autophagy, attempt to resolve toxic protein aggregates, which are common denominators of neurodegenerative diseases. In this issue of Genes & Development, Hetz and colleagues (pp. 2294 2306) surprisingly show that inhibition of the UPR by knockout of XBP-1 causes a massive increase in autophagy, enhances clearance of superoxide dismutase 1 (SOD1) aggregates, and delays the development of amyotrophic lateral sclerosis. These findings suggest the existence of a homeostatic-if not hormetic-balance between distinct cellular defense mechanisms.
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