The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
When ER stress reaches a dead end
Open accessAbstract
Endoplasmic reticulum (ER) stress is a common feature of several physiological and pathological conditions affecting the function of the secretory pathway. To restore ER homeostasis, an orchestrated signaling pathway is engaged that is known as the unfolded protein response (UPR). The UPR has a primary function in stress adaptation and cell survival; however, under irreversible ER stress a switch to pro-apoptotic signaling events induces apoptosis of damaged cells. The mechanisms that initiate ER stress-dependent apoptosis are not fully understood. Several pathways have been described where we highlight the participation of the BCL-2 family of proteins and ER calcium release. In addition, recent findings also suggest that microRNAs and oxidative stress are relevant players on the transition from adaptive to cell death programs. Here we provide a global and integrated overview of the signaling networks that may determine the elimination of a cell under chronic ER stress. This article is part of a Special Section entitled: Cell Death Pathways.
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Cites
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Self-citationEndoplasmic Reticulum Stress and the Hallmarks of Cancer
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Metadata
- Authors
- Urra, H., Dufey, E., Lisbona, F., Rojas-Rivera, D., & Hetz, C.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 1833
- Issue
- 12
- Pages
- 3507-3517
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W2023691970
- Cited by
- 457
- References
- 12
- FWCI
- 16.48
- Type
- journal article
- Language
- en
- Open access
- bronze
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