ArticleMolecules (Basel, Switzerland)2022
The RHIM of the Immune Adaptor Protein TRIF Forms Hybrid Amyloids with Other Necroptosis-Associated Proteins.
Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 21 citations in OpenAlex.
- Review
- Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Diffuse alveolar damage, acute respiratory distress syndrome (ARDS), and non-cardiogenic pulmonary edema (NCPE). Part 2: NCPE apart from ARDS, molecular and cellular consequences of primary injury to the lung interstitium, with comparative immunology of the dog and cat.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2026Review
- Toll-like receptor signaling outcome is determined by the stoichiometry of the endogenous TRIFosome.Science advances · 2026Article
- De novo cyclic peptides allow visualisation of the monomeric and functional amyloid conformations of the kinase RIPK3.The Biochemical journal · 2026Article
- Host Responses to SARS-CoV-2 with an Emphasis on Cytokines.International journal of molecular sciences · 2026Review
- Regulated cell death in sepsis-associated liver injury: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Necroptosis in asthma: a critical driver of immune dysregulation and airway remodeling.Frontiers in immunology · 2026Review
- Resonance assignments of the human receptor interacting protein kinase 1 (RIPK1) in its fibrillar conformation.Biomolecular NMR assignments · 2025Article
- Structural basis for amyloid fibril assembly by the master cell-signaling regulator receptor-interacting protein kinase 1.Nature communications · 2025Article
- Membrane charge primes the necroptotic kinase RIPK3 for amyloid assembly.Communications chemistry · 2025Article
- Necroptosis in obesity: a complex cell death event.Apoptosis : an international journal on programmed cell death · 2025Review
- PANoptosis: a new insight for oral diseases.Molecular biology reports · 2024Review
- HSPA8 inhibitors augment cancer chemotherapeutic effectiveness via potentiating necroptosis.Molecular biology of the cell · 2024Article
- Roles of RIPK1 as a stress sentinel coordinating cell survival and immunogenic cell death.Nature reviews. Molecular cell biology · 2023Review
- Review
- The role of RHIM in necroptosis.Biochemical Society transactions · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
TIR-domain-containing adapter-inducing interferon-β (TRIF) is an innate immune protein that serves as an adaptor for multiple cellular signalling outcomes in the context of infection. TRIF is activated via ligation of Toll-like receptors 3 and 4. One outcome of TRIF-directed signalling is the activation of the programmed cell death pathway necroptosis, which is governed by interactions between proteins that contain a RIP Homotypic Interaction Motif (RHIM). TRIF contains a RHIM sequence and can interact with receptor interacting protein kinases 1 (RIPK1) and 3 (RIPK3) to initiate necroptosis. Here, we demonstrate that the RHIM of TRIF is amyloidogenic and supports the formation of homomeric TRIF-containing fibrils. We show that the core tetrad sequence within the RHIM governs the supramolecular organisation of TRIF amyloid assemblies, although the stable amyloid core of TRIF amyloid fibrils comprises a much larger region than the conserved RHIM only. We provide evidence that RHIMs of TRIF, RIPK1 and RIPK3 interact directly to form heteromeric structures and that these TRIF-containing hetero-assemblies display altered and emergent properties that likely underlie necroptosis signalling in response to Toll-like receptor activation.
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.