ReviewJournal of Zhejiang University. Science. B
Molecular signal networks and regulating mechanisms of the unfolded protein response.
Review in Journal of Zhejiang University. Science. B. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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.
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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
60 citing papers in PubMed, 105 citations in OpenAlex.
- Acute hypoxia induces liver mitochondrial and endoplasmic reticulum stress in adult grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Article
- Hypertension and Diabetes Cooperatively Drive HSP90 Activation, HSP70 Suppression, and Left Ventricular Interstitial Expansion: Relevance to Maladaptive Myocardial Remodeling.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Meningeal lymphatic vessel dysfunction exacerbates brain injury in CVST mice via endoplasmic reticulum and oxidative stress pathways.Frontiers in immunology · 2026Article
- N6-methyladenosine modification of CBLB affects LPS-induced endoplasmic reticulum stress in alveolar epithelial cells.Central-European journal of immunology · 2026Article
- Unfolded protein response in bronchopulmonary dysplasia: mechanisms, pathways, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- New Role of Protein Misfolding Corrector in the ER Stress-Inflammation Axis: Possible Therapeutic Indication in Neuronal and Epithelial Tumor Cells.International journal of molecular sciences · 2025Article
- Nephrotoxicity of Phthalates: A Review Based on Epidemiological and Toxicological Evidence.Toxics · 2025Review
- C1QL1 inhibits breast cancer through the HSP90α/VCP-ERS/UPR axis.Experimental & molecular medicine · 2025Article
- MiR- 150 deletion promotes lung tumor growth by upregulating P-STAT3 and ROS in MDSCs.Scientific reports · 2025Article
- The role of autophagy in fibrosis: Mechanisms, progression and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Hepatitis B surface antigen: carcinogenesis mechanisms and clinical implications in hepatocellular carcinoma.Experimental hematology & oncology · 2025Review
- Nitroxidative Stress, Cell-Signaling Pathways, and Manganese Porphyrins: Therapeutic Potential in Neuropathic Pain.International journal of molecular sciences · 2025Review
- Hepatocellular carcinoma: pathogenesis, molecular mechanisms, and treatment advances.Frontiers in oncology · 2025Review
- Integration of Network Pharmacology, Molecular Docking, and Experimental Validation to Identify the Effect of EGCG on Alleviating Chondrocyte Inflammatory Damage by Targeting ER Stress-STAT3 Crosstalk.Journal of inflammation research · 2025Article
- Signaling Pathways Involved in Acute Pancreatitis.Journal of inflammation research · 2025Review
- L1, a 3,3'-diindolylmethane-derivative, induced ER stress-mediated apoptosis and suppressed growth through the FLI1/AKT pathway in erythroleukemia HEL cells.Frontiers in pharmacology · 2025Article
- The relationship between endoplasmic reticulum stress and apoptosis in the process of adipose-derived stromal cells differentiating into astrocytes.Cell adhesion & migration · 2024Article
- Implication of endoplasmic reticulum stress and mitochondrial perturbations in remote liver injury after renal ischemia/reperfusion in rats: potential protective role of azilsartan.Redox report : communications in free radical research · 2024Article
- Endothelial Unfolded Protein Response-Mediated Cytoskeletal Effects.Cell biochemistry and function · 2024Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Within the cell, several mechanisms exist to maintain homeostasis of the endoplasmic reticulum (ER). One of the primary mechanisms is the unfolded protein response (UPR). In this review, we primarily focus on the latest signal webs and regulation mechanisms of the UPR. The relationships among ER stress, apoptosis, and cancer are also discussed. Under the normal state, binding immunoglobulin protein (BiP) interacts with the three sensors (protein kinase RNA-like ER kinase (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1α (IRE1α)). Under ER stress, misfolded proteins interact with BiP, resulting in the release of BiP from the sensors. Subsequently, the three sensors dimerize and autophosphorylate to promote the signal cascades of ER stress. ER stress includes a series of positive and negative feedback signals, such as those regulating the stabilization of the sensors/BiP complex, activating and inactivating the sensors by autophosphorylation and dephosphorylation, activating specific transcription factors to enable selective transcription, and augmenting the ability to refold and export. Apart from the three basic pathways, vascular endothelial growth factor (VEGF)-VEGF receptor (VEGFR)-phospholipase C-γ (PLCγ)-mammalian target of rapamycin complex 1 (mTORC1) pathway, induced only in solid tumors, can also activate ATF6 and PERK signal cascades, and IRE1α also can be activated by activated RAC-alpha serine/threonine-protein kinase (AKT). A moderate UPR functions as a pro-survival signal to return the cell to its state of homeostasis. However, persistent ER stress will induce cells to undergo apoptosis in response to increasing reactive oxygen species (ROS), Ca
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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.