ArticleProceedings of the National Academy of Sciences of the United States of America2017
ER stress and distinct outputs of the IRE1α RNase control proliferation and senescence in response to oncogenic Ras.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
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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
58 citing papers in PubMed, 1 synthesis or guideline pooled it.
- ER stress as a trigger of UPR and ER-phagy in cancer growth and spread.Frontiers in oncology · 2022Pooled it
- Host-Pathogen Interaction as a Driver of Cellular Senescence: Microbial Triggers and Host Response.International journal of molecular sciences · 2026Review
- Proteostasis decline and endoplasmic reticulum stress in aging: Implications for cellular senescence and senescence-associated secretory phenotype regulation.Neural regeneration research · 2026Article
- Fatty acid channelling into triglycerides and oxylipins drives ferroptosis resistance during oncogenic BRAF-induced senescence.Cell death and differentiation · 2026Article
- Endoplasmic reticulum stress in disease pathogenesis: its implications for therapy.Signal transduction and targeted therapy · 2026Review
- Reduced osteogenic factors and early osteoblast senescence in SOD1(G93A) ALS mouse model.JCI insight · 2026Article
- K29-Linked Ubiquitination of Transcription Regulators Controls Cell Proliferation in the Unfolded Protein Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pharmacologic inhibition of IRE1α-dependent decay protects alveolar epithelial identity and prevents pulmonary fibrosis in mice.The Journal of clinical investigation · 2025Article
- Somatic mutations in IRE1α regulate keratinocyte migration and survival by differentially activating Rho GTPases.Journal of cell science · 2025Article
- Hyperoxia-induced senescence in fetal airway smooth muscle cells: role of mitochondrial reactive oxygen species and endoplasmic reticulum stress.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Glutamate promotes triple-negative breast cancer development through IRE1α/XBP1-mediated macrophage polarization: mechanism insights and therapy.Discover oncology · 2025Article
- Targeting ATF6α Attenuates UVB-Induced Senescence and Improves Skin Homeostasis by Regulating IL8 Expression.Aging cell · 2025Article
- Endoplasmic Reticulum Stress: Implications in Diseases.The protein journal · 2025Review
- Review
- Homeostasis control in health and disease by the unfolded protein response.Nature reviews. Molecular cell biology · 2025Review
- Endoplasmic Reticulum Stress in Cancer Progression: A Comprehensive Review of Its Role and Mechanisms.International journal of medical sciences · 2025Review
- Emerging role of IRE1α in vascular diseases.Journal of cell communication and signaling · 2024Review
- Endoplasmic reticulum stress-induced senescence in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Protein translation rate determines neocortical neuron fate.Nature communications · 2024Article
- ER-associated degradation adapter Sel1L is required for CD8Cell reports · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Oncogenic Ras causes proliferation followed by premature senescence in primary cells, an initial barrier to tumor development. The role of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in regulating these two cellular outcomes is poorly understood. During ER stress, the inositol requiring enzyme 1α (IRE1α) endoribonuclease (RNase), a key mediator of the UPR, cleaves
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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.