ArticleCell reports2020
A Molecular Mechanism for Turning Off IRE1α Signaling during Endoplasmic Reticulum Stress.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- Injury polarized CD4Redox biology · 2026Article
- RBM39 modulates UPR signaling through alternative splicing of IRE1α/Genes & development · 2026Article
- Dietary Myo-Inositol Improves Growth, Antioxidant and Immune Responses in Bisphenol S-Exposed Procambarus clarkii.Marine biotechnology (New York, N.Y.) · 2026Article
- The role of ER-associated degradation and ER-phagy in health and disease.Signal transduction and targeted therapy · 2026Review
- Adaptive-to-maladaptive IRE1α signaling as a driver of amyloidogenic APP processing in Alzheimer's disease.Frontiers in molecular biosciences · 2026Review
- Interplay of α-Synuclein Oligomers and Endoplasmic Reticulum Stress in Parkinson'S Disease: Insights into Cellular Dysfunctions.Inflammation · 2025Review
- RNA exosome-driven RNA processing instructs the duration of the unfolded protein response.Nucleic acids research · 2025Article
- Chaperone BiP controls ER stress sensor Ire1 through interactions with its oligomers.Life science alliance · 2024Article
- Congress of multiple dimers is needed for cross-phosphorylation of IRE1α and its RNase activity.Life science alliance · 2024Article
- UPF3B modulates endoplasmic reticulum stress through interaction with inositol-requiring enzyme-1α.Cell death & disease · 2024Article
- Endoplasmic Reticulum Membrane Homeostasis and the Unfolded Protein Response.Cold Spring Harbor perspectives in biology · 2024Review
- Cell-selective proteomics reveal novel effectors secreted by an obligate intracellular bacterial pathogen.Nature communications · 2024Article
- The Essential Functions of Molecular Chaperones and Folding Enzymes in Maintaining Endoplasmic Reticulum Homeostasis.Journal of molecular biology · 2024Review
- Article
- Exploring the IRE1 interactome: From canonical signaling functions to unexpected roles.The Journal of biological chemistry · 2024Review
- Endoplasmic reticulum stress-mediated cell death in cardiovascular disease.Cell stress & chaperones · 2024Review
- Navigating the landscape of mitochondrial-ER communication in health and disease.Frontiers in molecular biosciences · 2024Review
- Cell-selective proteomics reveal novel effectors secreted by an obligate intracellular bacterial pathogen.bioRxiv : the preprint server for biology · 2023Article
- Nascent Chain Ubiquitination is Uncoupled from Degradation to Enable Protein Maturation.bioRxiv : the preprint server for biology · 2023Article
- Signal sequence-triage is activated by translocon obstruction sensed by an ER stress sensor IRE1α.Cell structure and function · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Misfolded proteins in the endoplasmic reticulum (ER) activate IRE1α endoribonuclease in mammalian cells, which mediates XBP1 mRNA splicing to produce an active transcription factor. This promotes the expression of specific genes to alleviate ER stress, thereby attenuating IRE1α. Although sustained activation of IRE1α is linked to human diseases, it is not clear how IRE1α is attenuated during ER stress. Here, we identify that Sec63 is a subunit of the previously identified IRE1α/Sec61 translocon complex. We find that Sec63 recruits and activates BiP ATPase through its luminal J-domain to bind onto IRE1α. This leads to inhibition of higher-order oligomerization and attenuation of IRE1α RNase activity during prolonged ER stress. In Sec63-deficient cells, IRE1α remains activated for a long period of time despite the presence of excess BiP in the ER. Thus, our data suggest that the Sec61 translocon bridges IRE1α with Sec63/BiP to regulate the dynamics of IRE1α signaling in cells.
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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.