ArticleCell stress & chaperones2017
Moderate endoplasmic reticulum stress activates a PERK and p38-dependent apoptosis.
Article in Cell stress & chaperones, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- The pro-apoptotic GZMB and anti-apoptotic HAX-1 and DAD-1 genes and gene proteins in human right auricular tissue affected by coronary heart disease and aortic valve stenosis: a pilot study.Journal of molecular histology · 2026Article
- Molecular Mechanisms of Cadmium-Induced Apoptosis in Fish Cells: A Review.International journal of molecular sciences · 2026Review
- Mechanisms and Drug-Augmenting Strategies of Mesenchymal Stem Cells for Preserving β-Cell in Type 2 Diabetes.Drug design, development and therapy · 2026Review
- Surface Gene Mutations of Hepatitis B Virus and Related Pathogenic Mechanisms: A Narrative Review.Viruses · 2025Review
- Morbillivirus Canis Infection Induces Activation of Three Branches of Unfolded Protein Response, MAPK and Apoptosis.Viruses · 2024Article
- cFLIPCardiovascular drugs and therapy · 2023Article
- GSTO1 confers drug resistance in HCT‑116 colon cancer cells through an interaction with TNFαIP3/A20.International journal of oncology · 2022Article
- Unfolded Protein Response Differentially Modulates the Platelet Phenotype.Circulation research · 2022Article
- Extracellular Vesicle Therapy for Type 1 Diabetes.Frontiers in immunology · 2022Review
- KDELR2 knockdown synergizes with temozolomide to induce glioma cell apoptosis through the CHOP and JNK/p38 pathways.Translational cancer research · 2021Article
- Potential Roles of Endoplasmic Reticulum Stress and Cellular Proteins Implicated in Diabesity.Oxidative medicine and cellular longevity · 2021Review
- Depletion of eukaryotic initiation factor 5B (eIF5B) reprograms the cellular transcriptome and leads to activation of endoplasmic reticulum (ER) stress and c-Jun N-terminal kinase (JNK).Cell stress & chaperones · 2021Article
- The Role of Molecular Chaperones in Virus Infection and Implications for Understanding and Treating COVID-19.Journal of clinical medicine · 2020Review
- Cross organelle stress response disruption promotes gentamicin-induced proteotoxicity.Cell death & disease · 2020Article
- Regulation of senescence traits by MAPKs.GeroScience · 2020Review
- Mesenchymal stem cell-derived exosomes protect beta cells against hypoxia-induced apoptosis via miR-21 by alleviating ER stress and inhibiting p38 MAPK phosphorylation.Stem cell research & therapy · 2020Article
- Naturally Occurring Hepatitis B Virus Mutations Leading to Endoplasmic Reticulum Stress and Their Contribution to the Progression of Hepatocellular Carcinoma.International journal of molecular sciences · 2019Review
- Endoplasmic Reticulum Stress Activates Unfolded Protein Response Signaling and Mediates Inflammation, Obesity, and Cardiac Dysfunction: Therapeutic and Molecular Approach.Frontiers in pharmacology · 2019Review
- Protein kinase R-like endoplasmatic reticulum kinase is a mediator of stretch in ventilator-induced lung injury.Respiratory research · 2018Article
- Functional expression of TLR5 of different vertebrate species and diversification in intestinal pathogen recognition.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The endoplasmic reticulum (ER) has the ability to signal organelle dysfunction via a complex signaling network known as the unfolded protein response (UPR). In this work, hamster fibroblast cells exhibiting moderate levels of ER stress were compared to those exhibiting severe ER stress. Inhibition of N-linked glycosylation was accomplished via a temperature-sensitive mutation in the Dad1 subunit of the oligosaccharyltransferase (OST) complex or by direct inhibition with tunicamycin (Tm). Temperature shift (TS) treatment generated weak activation of ER stress signaling when compared to doses of Tm that are typically used in ER stress studies (500-1000 nM). A dose-response analysis of key ER stress signaling mediators, inositol-requiring enzyme 1 (IRE1) and protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), revealed 20-40 nM of Tm to generate activation intensity similar to TS treatment. In parental BHK21 cells, moderate (20-40 nM) and high doses (200-1000 nM) of Tm were compared to identify physiological and signaling-based differences in stress response. Inhibition of ER Ca
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