ArticleCellular and molecular life sciences : CMLS2017
Death receptor 3 mediates necroptotic cell death.
Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 35 citations in OpenAlex.
- Cerebrospinal fluid biomarkers link toxic astrogliosis and microglial activation to multiple sclerosis severity.Multiple sclerosis and related disorders · 2019Trial
- Article
- Porcine Epidemic Diarrhea-Virus-Induced Cell Death: Mechanistic Insights and Therapeutic Strategies.Veterinary sciences · 2025Review
- The Role of Post-Translational Modifications in Necroptosis.Biomolecules · 2025Review
- TRAF2 and RIPK1 redundantly mediate classical NFκB signaling by TNFR1 and CD95-type death receptors.Cell death & disease · 2025Article
- Pharmacological mechanisms and therapeutic prospects of plant metabolites from traditional Chinese medicine in regulating programmed cell death in Alzheimer's disease.Frontiers in pharmacology · 2025Review
- Necroptosis plays a role in TL1A-induced airway inflammation and barrier damage in asthma.Respiratory research · 2024Article
- ZBP1 and TRIF trigger lethal necroptosis in mice lacking caspase-8 and TNFR1.Cell death and differentiation · 2024Article
- Death receptor 3 is involved in preeclampsia through regulating placental trophoblast cell physiology by inactivating the PI3K/AKT pathway.Immunity, inflammation and disease · 2023Article
- Role of TL1A in Inflammatory Autoimmune Diseases: A Comprehensive Review.Frontiers in immunology · 2022Review
- Necroptosis molecular mechanisms: Recent findings regarding novel necroptosis regulators.Experimental & molecular medicine · 2021Review
- TL1A-DR3 Plasma Levels Are Predictive of HIV-1 Disease Control, and DR3 Costimulation Boosts HIV-1-Specific T Cell Responses.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- TL1A regulates adipose-resident innate lymphoid immune responses and enables diet-induced obesity in mice.International journal of obesity (2005) · 2020Article
- Fucoidan Induces Apoptosis of HT-29 Cells via the Activation of DR4 and Mitochondrial Pathway.Marine drugs · 2020Article
- Functional roles in cell signaling of adaptor protein TRADD from a structural perspective.Computational and structural biotechnology journal · 2020Review
- The Cancer Genome Atlas dataset-based analysis of aberrantly expressed genes by GeneAnalytics in thymoma associated myasthenia gravis: focusing on T cells.Journal of thoracic disease · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Death receptor 3 (DR3) was initially identified as a T cell co-stimulatory and pro-inflammatory molecule, but further studies revealed a more complex role of DR3 and its ligand TL1A. Although being a death receptor, DR3 gained to date predominantly attention as a contributor to inflammation-driven diseases. In our study, we investigated the cell death pathways associated with DR3. We show that in addition to apoptosis, DR3 can robustly trigger necroptotic cell death and provide evidence for TL1A-induced, DR3-mediated necrosome assembly. DR3-mediated necroptosis critically depends on receptor-interacting protein 1 (RIP1) and RIP3, the core components of the necroptotic machinery, which activate the pseudo-kinase mixed lineage kinase domain-like, the prototypic downstream effector molecule of necroptosis. Moreover, we demonstrate that DR3-mediated necroptotic cell death is accompanied by, but does not depend on generation of reactive oxygen species. In sum, we identify DR3 as a novel necroptosis-inducing death receptor and thereby lay ground for elucidating the (patho-) physiological relevance of DR3-mediated necroptotic cell death in vitro and in vivo.
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.