ReviewCell death & disease2015
Protein kinase R-like ER kinase and its role in endoplasmic reticulum stress-decided cell fate.
Review in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 1 of them a synthesis that pooled it.
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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
165 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Medical Gas Therapy for Tissue, Organ, and CNS Protection: A Systematic Review of Effects, Mechanisms, and Challenges.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Pooled it
- From Cellular Stress to Systemic Adaptation: The Circadian Clock and Stress Response at Cellular and Systemic Levels.International journal of molecular sciences · 2026Review
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Low-Intensity Extracorporeal Shock Wave Therapy Restores Passive Urethral Closure Mechanism in Vaginal Distension Rat Model.International urogynecology journal · 2026Article
- Chrysosplenetin-induced TMED3 aggregation triggers unfolded protein response in pancreatic cancer.EMBO molecular medicine · 2026Article
- Heavy metal toxicity as a driver of endoplasmic reticulum stress and dysfunction.The FEBS journal · 2026Review
- Differential Effects of PERK and IRE1α Silencing on Expression of Apoptosis and Autophagy Markers in T-Lymphoblastic Leukemia MOLT-3 Cells.International journal of molecular sciences · 2026Article
- Matrix stiffness induced CREB3L1 activation contributed to skin fibrosis through calcium influx triggered endoplasmic reticulum stress.Cellular and molecular life sciences : CMLS · 2026Article
- Stromal homeostasis-restoring "rocket-like" nanomedicine inhibited pancreatic tumor growth in vivo.Materials today. Bio · 2026Article
- Holistic therapeutic philosophy: Boost a cascade communication between endoplasmic reticulum-mitochondria-lysosome to overload intracellular CaMaterials today. Bio · 2026Article
- Mitochondrial dysfunction in type 1 diabetes and its implications for pancreatic beta-cell survival and insulin secretion.Acta diabetologica · 2026Review
- COL12A1 rs970547 Polymorphism Predisposes Anterior Cruciate Ligament Injury by Inducing ER Stress and Impairing Fibroblast Function.Advanced biology · 2026Article
- The Molecular Architecture of Neurodegeneration: An Integrative Overview of Convergent Mechanisms.NeuroSci · 2026Review
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- Review
- Inhibition of calreticulin by protein nanoparticles carrying antisense oligonucleotides reduce gene expression and infection ofNanomedicine (London, England) · 2025Article
- ER stress tolerance is regulated by copper-dependent PERK kinase activity.Cell reports · 2025Article
- Review
- Genetic and Pharmacological Inhibition of NOX4 Protects Against Rhabdomyolysis-Induced Acute Kidney Injury Through Suppression of Endoplasmic Reticulum Stress.Antioxidants (Basel, Switzerland) · 2025Article
- Glutaminase inhibition ameliorates cancer-associated fibroblast lipid support of pancreatic cancer cell growth.Cancer & metabolism · 2025Article
105 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past few decades, understandings and evidences concerning the role of endoplasmic reticulum (ER) stress in deciding the cell fate have been constantly growing. Generally, during ER stress, the signal transductions are mainly conducted by three ER stress transducers: protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring kinase 1 (IRE1) and activating transcription factor 6 (ATF6). Consequently, the harmful stimuli from the ER stress transducers induce apoptosis and autophagy, which share several crosstalks and eventually decide the cell fate. The dominance of apoptosis or autophagy induced by ER stress depends on the type and degree of the stimuli. When ER stress is too severe and prolonged, apoptosis is induced to eliminate the damaged cells; however, when stimuli are mild, cell survival is promoted to maintain normal physiological functions by inducing autophagy. Although all the three pathways participate in ER stress-induced apoptosis and autophagy, PERK shows several unique characteristics by interacting with some specific downstream effectors. Notably, there are some preliminary findings on PERK-dependent mechanisms switching autophagy and apoptosis. In this review, we particularly focused on the novel, intriguing and complicated role of PERK in ER stress-decided cell fate, and also discussed more roles of PERK in restoring cellular homeostasis. However, more in-depth knowledge of PERK in the future would facilitate our understanding about many human diseases and benefit in searching for new molecular therapeutic targets.
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