ArticleJournal of cell science2013
The ire-1 ER stress-response pathway is required for normal secretory-protein metabolism in C. elegans.
Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 72 citations in OpenAlex.
- Review
- ER stress tolerance is regulated by copper-dependent PERK kinase activity.Cell reports · 2025Article
- Loss of FIC-1-mediated AMPylation activates the UPRER and upregulates cytosolic HSP70 chaperones to suppress polyglutamine toxicity.PLoS genetics · 2025Article
- HLH-30/TFEB Rewires the Chaperone Network to Promote Proteostasis Upon Perturbations to the Coenzyme A and Iron-Sulfur Cluster Biosynthesis Pathways.Aging cell · 2025Article
- Immunity-linked genes are stimulated by a membrane stress pathway linked to Golgi function and the ARF-1 GTPase.Science advances · 2023Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- The unfolded protein response transcription factor XBP1s ameliorates Alzheimer's disease by improving synaptic function and proteostasis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Endoplasmic Reticulum in Metaplasticity: From Information Processing to Synaptic Proteostasis.Molecular neurobiology · 2022Review
- Melatonin reduces the endoplasmic reticulum stress and polyubiquitinated protein accumulation induced by repeated anesthesia exposure in Caenorhabditis elegans.Scientific reports · 2022Article
- The Unfolded Protein Responses in Health, Aging, and Neurodegeneration: Recent Advances and Future Considerations.Frontiers in molecular neuroscience · 2022Review
- A putative long noncoding RNA-encoded micropeptide maintains cellular homeostasis in pancreatic β cells.Molecular therapy. Nucleic acids · 2021Article
- Sirtuins and Autophagy in Age-Associated Neurodegenerative Diseases: Lessons from theInternational journal of molecular sciences · 2021Review
- Global Proteotoxicity Caused by Human βInternational journal of molecular sciences · 2021Article
- Neuronal regulatedeLife · 2021Article
- Inactivation of theAutophagy · 2021Article
- Endoplasmic reticulum stress/XBP1 promotes airway mucin secretion under the influence of neutrophil elastase.International journal of molecular medicine · 2021Article
- Role of Unfolded Protein Response and Endoplasmic Reticulum-Associated Degradation by Repeated Exposure to Inhalation Anesthetics inInternational journal of medical sciences · 2021Article
- Endoplasmic Reticulum Homeostasis and Stress Responses in Caenorhabditis elegans.Progress in molecular and subcellular biology · 2021Article
- Insulin-like growth factor 2 (IGF2) protects against Huntington's disease through the extracellular disposal of protein aggregates.Acta neuropathologica · 2020Article
- ENPL-1, theDevelopment (Cambridge, England) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The unfolded protein response (UPR) allows cells to cope with endoplasmic reticulum (ER) stress by adjusting the capacity of the ER to the load of ER-associated tasks. The UPR is important for maintaining ER homeostasis under extreme ER stress. UPR genes are important under normal growth conditions as well, but what they are required for under these conditions is less clear. Using C. elegans, we show that the ire-1/xbp-1 arm of the UPR plays a crucial role in maintaining ER plasticity and function also in the absence of external ER stress. We find that during unstressed growth conditions, loss of ire-1 or xbp-1 compromises basic ER functions required for the metabolism of secreted proteins, including translation, folding and secretion. Notably, by compromising ER-associated degradation (ERAD) and phagocytosis, loss of ire-1 hinders the clearance of misfolded proteins from the ER as well as the clearance of proteins that were secreted into the pseudocoleom. Whereas the basal activity of the UPR is beneficial under normal conditions, it accelerates the pathology caused by toxic Aβ protein in a C. elegans model of Alzheimer's disease. Taken together, our findings indicate that UPR genes are critical for maintaining secretory protein metabolism under normal growth conditions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.