ArticleNature communications2017
Fortilin binds IRE1α and prevents ER stress from signaling apoptotic cell death.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
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Who cites it
39 citing papers in PubMed, 78 citations in OpenAlex.
- Pharmacological Modulators of TCTP: Opportunities and Challenges for Drug Repurposing.International journal of molecular sciences · 2026Review
- Fortilin binds and stabilizes MEF2C, activates it through phosphorylation, and drives transcription of the cell structural and survival protein CTNNA3.The Journal of biological chemistry · 2026Article
- Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.Communications biology · 2025Article
- Fortilin binds CTNNA3 and protects it against phosphorylation, ubiquitination, and proteasomal degradation to guard cells against apoptosis.Communications biology · 2025Article
- Signaling Pathways Involved in Acute Pancreatitis.Journal of inflammation research · 2025Review
- Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025Review
- Significance of Programmed Cell Death Pathways in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- UPF3B modulates endoplasmic reticulum stress through interaction with inositol-requiring enzyme-1α.Cell death & disease · 2024Article
- Biological role and expression of translationally controlled tumor protein (TCTP) in tumorigenesis and development and its potential for targeted tumor therapy.Cancer cell international · 2024Review
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- Hepatic progesterone receptor membrane component 1 attenuates ethanol-induced liver injury by reducing acetaldehyde production and oxidative stress.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Deubiquitylase OTUD3 Mediates Endoplasmic Reticulum Stress through Regulating Fortilin Stability to Restrain Dopaminergic Neurons Apoptosis.Antioxidants (Basel, Switzerland) · 2023Article
- Enhanced IRE1α Phosphorylation/Oligomerization-Triggered XBP1 Splicing Contributes to Parkin-Mediated Prevention of SH-SY5Y Cell Death under Nitrosative Stress.International journal of molecular sciences · 2023Article
- Role of Translationally Controlled Tumor Protein (TCTP) in the Development of Hypertension and Related Diseases in Mouse Models.Biomedicines · 2022Review
- Review
- IRE1/XBP1 and endoplasmic reticulum signaling - from basic to translational research for cardiovascular disease.Current opinion in physiology · 2022Article
- The ER-Mitochondria Interface as a Dynamic Hub for T Cell Efficacy in Solid Tumors.Frontiers in cell and developmental biology · 2022Review
- IRE1 signaling regulates chondrocyte apoptosis and death fate in the osteoarthritis.Journal of cellular physiology · 2022Review
- Expression and purification of a cleavable recombinant fortilin from Escherichia coli for structure activity studies.Protein expression and purification · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The endoplasmic reticulum, the cytoplasmic organelle that matures a massive amount of nascent secretory polypeptides, is particularly sensitive to stress. Endoplasmic reticulum stress causes unfolded proteins to populate the organelle, eliciting the unfolded protein response. During the unfolded protein response, GRP78-an endoplasmic reticulum master stress regulator-detaches from three endoplasmic reticulum stress sensors (IRE1α, PERK, and ATF6) and allows them to activate the apoptotic signaling pathway. Fortilin, a pro-survival molecule, is known to inhibit apoptosis by binding and inhibiting p53, but its role in endoplasmic reticulum stress-induced apoptosis remains unknown. Here, we report that fortilin directly interacts with the cytoplasmic domain of IRE1α, inhibits both kinase and endoribonuclease (RNase) activities of the stress sensor, and protects cells against apoptotic cell death at both cellular and whole animal levels. Our data support a role of fortilin in the unfolded protein response and its potential participation in human diseases caused by unfolded protein response.IRE1α is an ER stress sensor, whose activity induces apoptosis. Here, the authors report that fortilin, a pro-survival factor, with yet unknown roles in ER stress, interacts with active IRE1α, inhibits both its kinase end RNase activities, and protects cells from apoptosis both in vitro and in vivo.
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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.