ReviewF1000Research2017
Recent insights into PERK-dependent signaling from the stressed endoplasmic reticulum.
Review in F1000Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
55 citing papers in PubMed, 106 citations in OpenAlex.
- Endothelial PERK restricts lymphoid regeneration by reducing DLL4-NOTCH3 signaling at the Pre-B niche.Cell reports · 2026Article
- Heavy metal toxicity as a driver of endoplasmic reticulum stress and dysfunction.The FEBS journal · 2026Review
- Article
- Imaging mass cytometry unveils functional and spatial remodeling of peri-lesional cells in jaw osteonecrosis.Communications biology · 2026Article
- Sida Rhombifolia linn: an empirical analysis on phytochemicals and an in vitro outcome on anti-inflammatory and antioxidant perspective.Scientific reports · 2025Article
- Activation of the PERK Branch of the UPR as a Strategy for Improving Outcomes in Acute Ischemic Stroke.ACS omega · 2025Article
- p.Phe508del-CFTR Trafficking: A Protein Quality Control Perspective Through UPR, UPS, and Autophagy.International journal of molecular sciences · 2025Review
- PERK-Olating Through Cancer: A Brew of Cellular Decisions.Biomolecules · 2025Review
- Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025Review
- Quantitative proteomics reveals the mechanism of endoplasmic reticulum stress-mediated pulmonary fibrosis in mice.Heliyon · 2024Article
- Activating transcription factor 4 plays a major role in shaping the transcriptional response to isoginkgetin in HCT116 cells.Scientific reports · 2024Article
- Updated mechanisms of MASLD pathogenesis.Lipids in health and disease · 2024Review
- The unfolded protein response of the endoplasmic reticulum protects Caenorhabditis elegans against DNA damage caused by stalled replication forks.G3 (Bethesda, Md.) · 2024Article
- Article
- MAM-mediated mitophagy and endoplasmic reticulum stress: the hidden regulators of ischemic stroke.Frontiers in cellular neuroscience · 2024Review
- Unfolded protein responses in T cell immunity.Frontiers in immunology · 2024Review
- Lithium chloride induces apoptosis by activating endoplasmic reticulum stress in pancreatic cancer.Translational oncology · 2023Article
- Regulation of the unfolded protein response during dehydration stress in African clawed frogs, Xenopus laevis.Cell stress & chaperones · 2023Article
- Article
- Endoplasmic Reticulum Stress in the Brain Tumor Immune Microenvironment.Molecular cancer research : MCR · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The unfolded protein response (UPR) is an evolutionarily conserved stress response to intra- and extracellular conditions that disrupt endoplasmic reticulum (ER) protein-folding capacity. The UPR is engaged by a variety of disease conditions, including most cancers as well as both metabolic and neurodegenerative disorders. Three transmembrane transducers-PERK, IRE1, and ATF6-are responsible for activating downstream signaling pathways that mediate the UPR and subsequent stress response pathways. PERK, an ER resident transmembrane protein kinase, initiates both pro-apoptotic and pro-survival signaling pathways. In the context of neoplasia, PERK and its downstream targets alter gene expression that can be both pro- and anti-tumorigenic. In this review, we discuss recent advances in understanding how canonical and non-canonical PERK-mediated signaling pathways influence cell fate, tumor progression, and tumor suppression and avenues for therapeutic intervention.
Indexed as
Identifiers
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.