ReviewBiotechnology and bioengineering2011
A review of the mammalian unfolded protein response.
Review in Biotechnology and bioengineering, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
199 citing papers in PubMed, 405 citations in OpenAlex.
- Autophagy prevents ER stress-induced Tight Junction barrier disruption via claudin-2 homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Selective activation of the unfolded protein response and proteolytic pathways in sarcopenic limb muscles of bronchiectasis patients.ERJ open research · 2026Article
- Deletion of CHOP in beta cell protects mice from cardiovascular complications in type 2 diabetes: evidence from a pre-clinical mouse model.Journal of molecular and cellular cardiology plus · 2025Article
- ATF6 and pS6K as prognostic biomarkers in newly diagnosed diffuse large B-cell lymphoma.Scientific reports · 2025Article
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- ATF6 enables pathogen infection in ticks by inducingProceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2.Biomolecules · 2025Review
- iPAR: a new reporter for eukaryotic cytoplasmic protein aggregation.BMC methods · 2025Article
- Analysis of Endoplasmic Reticulum Stress-Associated Proteins As Prognostic Markers In Breast Cancer.Current genomics · 2025Article
- PTGS2/GRP78 Activation Triggers Endoplasmic Reticulum Stress Leading to Lipid Metabolism Disruption and Cell Apoptosis, Exacerbating Damage in Bovine Mastitis.Biomolecules · 2024Article
- Chronic Corticosterone Administration-Induced Mood Disorders in Laboratory Rodents: Features, Mechanisms, and Research Perspectives.International journal of molecular sciences · 2024Review
- Antioxidants and Mechanistic Insights for Managing Dry Age-Related Macular Degeneration.Antioxidants (Basel, Switzerland) · 2024Review
- Naturally occurring small molecules with dual effect upon inflammatory signaling pathways and endoplasmic reticulum stress response.Journal of physiology and biochemistry · 2024Article
- Increased ER Stress and Unfolded Protein Response Activation in Epithelial and Inflammatory Cells in Hypersensitivity Pneumonitis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Article
- Understanding the Unfolded Protein Response (UPR) Pathway: Insights into Neuropsychiatric Disorders and Therapeutic Potentials.Biomolecules & therapeutics · 2024Review
- Benefits and Pitfalls of a Glycosylation Inhibitor Tunicamycin in the Therapeutic Implication of Cancers.Cells · 2024Review
- Nitrogen-doped carbon quantum dot regulates cell proliferation and differentiation by endoplasmic reticulum stress.Animal cells and systems · 2024Article
139 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Proteins requiring post-translational modifications such as N-linked glycosylation are processed in the endoplasmic reticulum (ER). A diverse array of cellular stresses can lead to dysfunction of the ER and ultimately to an imbalance between protein-folding capacity and protein-folding load. Cells monitor protein folding by an inbuilt quality control system involving both the ER and the Golgi apparatus. Unfolded or misfolded proteins are tagged for degradation via ER-associated degradation (ERAD) or sent back through the folding cycle. Continued accumulation of incorrectly folded proteins can also trigger the unfolded protein response (UPR). In mammalian cells, UPR is a complex signaling program mediated by three ER transmembrane receptors: activating transcription factor 6 (ATF6), inositol requiring kinase 1 (IRE1) and double-stranded RNA-activated protein kinase (PKR)-like endoplasmic reticulum kinase (PERK). UPR performs three functions, adaptation, alarm, and apoptosis. During adaptation, the UPR tries to reestablish folding homeostasis by inducing the expression of chaperones that enhance protein folding. Simultaneously, global translation is attenuated to reduce the ER folding load while the degradation rate of unfolded proteins is increased. If these steps fail, the UPR induces a cellular alarm and mitochondrial mediated apoptosis program. UPR malfunctions have been associated with a wide range of disease states including tumor progression, diabetes, as well as immune and inflammatory disorders. This review describes recent advances in understanding the molecular structure of UPR in mammalian cells, its functional role in cellular stress, and its pathophysiology.
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What OpenQuestion holds
Registered trials
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.