ArticleStructure (London, England : 1993)2014
Mechanistic basis for functional promiscuity in the TNF and TNF receptor superfamilies: structure of the LIGHT:DcR3 assembly.
Article in Structure (London, England : 1993), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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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
26 citing papers in PubMed, 33 citations in OpenAlex.
- Realizing the potential of agonistic antibody immunotherapy.Nature reviews. Drug discovery · 2026Review
- The Therapeutic Potential of Targeting TL1A in a Spectrum of Inflammatory Disorders.Journal of inflammation research · 2026Review
- Evaluation of LIGHT-derived peptides to disrupt the HVEM/LIGHT immune checkpoint.Scientific reports · 2025Article
- CD95/Fas stoichiometry in future precision medicine.Cell death and differentiation · 2025Review
- Aging-related biomarker discovery in the era of immune checkpoint inhibitors for cancer patients.Frontiers in immunology · 2024Review
- A stable, engineered TL1A ligand co-stimulates T cells via specific binding to DR3.Scientific reports · 2022Article
- Realigning the LIGHT signaling network to control dysregulated inflammation.The Journal of experimental medicine · 2022Article
- Receptor Specificity Engineering of TNF Superfamily Ligands.Pharmaceutics · 2022Review
- Structural delineation and phase-dependent activation of the costimulatory CD27:CD70 complex.The Journal of biological chemistry · 2021Article
- TNF receptor agonists induce distinct receptor clusters to mediate differential agonistic activity.Communications biology · 2021Article
- A Systematic Test of Receptor Binding Kinetics for Ligands in Tumor Necrosis Factor Superfamily by Computational Simulations.International journal of molecular sciences · 2020Article
- A computational model for understanding the oligomerization mechanisms of TNF receptor superfamily.Computational and structural biotechnology journal · 2020Article
- Role of TGFβ3-Smads-Sp1 axis in DcR3-mediated immune escape of hepatocellular carcinoma.Oncogenesis · 2019Article
- Structural Basis of CD160:HVEM Recognition.Structure (London, England : 1993) · 2019Article
- Expression and Clinical Significance of Decoy Receptor 3 in Acute-on-Chronic Liver Failure.BioMed research international · 2019Article
- Structure of the 4-1BB/4-1BBL complex and distinct binding and functional properties of utomilumab and urelumab.Nature communications · 2018Article
- Crystal structure of the human 4-1BB/4-1BBL complex.The Journal of biological chemistry · 2018Article
- Anti-apoptosis Effect of Decoy Receptor 3 in Cholangiocarcinoma Cell Line TFK-1.Chinese medical journal · 2018Article
- Mechanisms of immunomodulation by mammalian and viral decoy receptors: insights from structures.Nature reviews. Immunology · 2017Review
- DcR3 gene polymorphisms are associated with sporadic breast infiltrating ductal carcinoma in Northeast Chinese women.Oncotarget · 2016Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
LIGHT initiates intracellular signaling via engagement of the two TNF receptors, HVEM and LTβR. In humans, LIGHT is neutralized by DcR3, a unique soluble member of the TNFR superfamily, which tightly binds LIGHT and inhibits its interactions with HVEM and LTβR. DcR3 also neutralizes two other TNF ligands, FasL and TL1A. Due to its ability to neutralize three distinct different ligands, DcR3 contributes to a wide range of biological and pathological processes, including cancer and autoimmune diseases. However, the mechanisms that support the broad specificity of DcR3 remain to be fully defined. We report the structures of LIGHT and the LIGHT:DcR3 complex, which reveal the structural basis for the DcR3-mediated neutralization of LIGHT and afford insights into DcR3 function and binding promiscuity. Based on these structures, we designed LIGHT mutants with altered affinities for DcR3 and HVEM, which may represent mechanistically informative probe reagents.
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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.