ArticleNature2016
NOD1 and NOD2 signalling links ER stress with inflammation.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 323 papers.
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Who cites it
323 citing papers in PubMed, 509 citations in OpenAlex.
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- Unconventional role of hydroxymethylglutaryl-CoA synthase 1 in driving pathogenic TScience advances · 2026Article
- Integrated molecular mechanisms of salinity response in Apostichopus japonicus: focus on miRNA-driven core pathways and target gene regulation.Marine biotechnology (New York, N.Y.) · 2026Review
- Endoplasmic Reticulum Stress-Induced Endothelial Cell Pyroptosis Contributes to Pulmonary Vascular Remodeling and Pulmonary Arterial Hypertension via IRE1α/Caspase-3/GSDME Pathway.Journal of the American Heart Association · 2026Article
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Comparative Transcriptome Analysis of the Abdominal Ganglion Reveals Molecular Networks and Key Genes Underlying Thermal Tolerance in Red Swamp Crayfish (Animals : an open access journal from MDPI · 2026Article
- Mechanical ventilation activates PERK/eIF2α and NOD1 pathways that contribute to NF-κB-driven inflammation in VILI.Respiratory research · 2026Article
- Death-associated protein kinase 2 (DAPK2) propagates endoplasmic reticulum stress in macrophages to worsen sepsis through HSPA5-IRE1α axis.Molecular biomedicine · 2026Article
- Simultaneous NOD1 and NOD2 Deletion in Hematopoietic Stem and Progenitor cells Promotes Long-Term Donor Chimerism.Transplantation and cellular therapy · 2026Article
- Metabolic orchestration of NOD1 signaling by AMPK-mediated phosphorylation of ZDHHC5.iScience · 2026Article
- Low-dose TNF-α drives malignant progression and lipid metabolism in glioblastoma through the TRAF2-FASN axis.Cell death discovery · 2026Article
- Stable serum peptidoglycan fragment levels do not support leaky gut in the acute phase or at one month following "mild" traumatic brain injury: A preliminary study.Brain, behavior, & immunity - health · 2026Article
- Article
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- BvrR From Brucella abortus Induces Neuroinflammation Through IRE1-Mediated Activation of ATF2 and NF-κB.MicrobiologyOpen · 2026Article
- Brucella abortus infection exploits ZDHHC3-mediated STAT3 palmitoylation to regulate host responses and promote persistence.Veterinary research · 2026Article
- Transcutaneous electrical nerve stimulation treated anterior talo-fibular ligament injured rat through the gut-joint axis and intestinal microbiota.Frontiers in microbiology · 2026Article
- Endoplasmic reticulum stress as a mechanistic link between nutrition and inflammatory bowel disease.Frontiers in nutrition · 2026Review
263 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) stress is a major contributor to inflammatory diseases, such as Crohn disease and type 2 diabetes. ER stress induces the unfolded protein response, which involves activation of three transmembrane receptors, ATF6, PERK and IRE1α. Once activated, IRE1α recruits TRAF2 to the ER membrane to initiate inflammatory responses via the NF-κB pathway. Inflammation is commonly triggered when pattern recognition receptors (PRRs), such as Toll-like receptors or nucleotide-binding oligomerization domain (NOD)-like receptors, detect tissue damage or microbial infection. However, it is not clear which PRRs have a major role in inducing inflammation during ER stress. Here we show that NOD1 and NOD2, two members of the NOD-like receptor family of PRRs, are important mediators of ER-stress-induced inflammation in mouse and human cells. The ER stress inducers thapsigargin and dithiothreitol trigger production of the pro-inflammatory cytokine IL-6 in a NOD1/2-dependent fashion. Inflammation and IL-6 production triggered by infection with Brucella abortus, which induces ER stress by injecting the type IV secretion system effector protein VceC into host cells, is TRAF2, NOD1/2 and RIP2-dependent and can be reduced by treatment with the ER stress inhibitor tauroursodeoxycholate or an IRE1α kinase inhibitor. The association of NOD1 and NOD2 with pro-inflammatory responses induced by the IRE1α/TRAF2 signalling pathway provides a novel link between innate immunity and ER-stress-induced inflammation.
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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.