ReviewApplied microbiology and biotechnology2021
Integrated signaling system under endoplasmic reticulum stress in eukaryotic microorganisms.
Review in Applied microbiology and biotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Endoplasmic reticulum autophagy in inflammatory diseases.Frontiers in immunology · 2026Review
- Curcumin Attenuates Fumonisin B1-Induced PK-15 Cell Apoptosis by Upregulating miR-1249 Expression to Inhibit the IRE1/MKK7/JNK/CASPASE3 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- IRE1α modulates M1 oncolytic virus sensitivity via ER stress regulation in bladder cancer.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- Treponema pallidum recombinant protein Tp0768 enhances the ability of HUVECs to promote neutrophil chemotaxis through the TLR2/ER stress signaling pathway.Journal of leukocyte biology · 2024Article
- Endoplasmic reticulum stress-a key guardian in cancer.Cell death discovery · 2024Review
- Insights into the Activation of Unfolded Protein Response Mechanism during Coronavirus Infection.Current issues in molecular biology · 2024Review
- Review
- Finding New Targets for the Treatment of Heart Failure: Endoplasmic Reticulum Stress and Autophagy.Journal of cardiovascular translational research · 2023Review
- Ola1p trafficking indicates an interaction network between mitochondria, lipid droplets, and stress granules in times of stress.Journal of lipid research · 2023Article
- Endoplasmic Reticulum Stress in Elderly Patients with COVID-19: Potential of Melatonin Treatment.Viruses · 2023Review
- Zinc Oxide Particles Can Cause Ovarian Toxicity by Oxidative Stress in Female Mice Model.International journal of nanomedicine · 2022Article
- Autoantibodies in the pathogenesis of idiopathic inflammatory myopathies: Does the endoplasmic reticulum stress response have a role?Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The endoplasmic reticulum (ER) is a multifunctional organelle, which is crucial for correct folding and assembly of secretory and transmembrane proteins. Perturbations of ER function can cause ER stress. ER stress can activate the unfolded protein response (UPR) to cope with the accumulation of misfolded proteins and protein toxicity. UPR is a coordination system that regulates transcription and translation, leading to the recovery of ER homeostasis or cell death. However, cells have an integrated signaling system to cope with ER stress, which helps cells to restore and balance their ER function. The main components of this system are ER-associated degradation (ERAD), autophagy, hypoxia signaling, and mitochondrial biogenesis. If the balance cannot be restored, the imbalance will lead to cell death or apoptosis, or even to a series of diseases. In this review, a series of activities to restore the homeostasis of cells during ER stress are discussed. KEY POINTS: • Endoplasmic reticulum (ER) plays a key role in the biological process of cells. • Perturbations of ER function can cause ER stress, including the ER overload response (EOR), sterol-regulated cascade reaction, and the UPR. • Cells have an integrated signaling system (ERAD, autophagy, hypoxia signaling, and mitochondrial biogenesis) to cope with the adverse impact caused by ER stress.
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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.