ArticleCurrent pharmacology reports2018
TRAF molecules in inflammation and inflammatory diseases.
Article in Current pharmacology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.
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
60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 130 citations in OpenAlex.
- The genomic architecture of circulating cytokine levels points to drug targets for immune-related diseases.Communications biology · 2025Pooled it
- Systematic Review and Meta-analysis of Peripheral Blood DNA Methylation Studies in Inflammatory Bowel Disease.Journal of Crohn's & colitis · 2023Pooled it
- Emerging perspectives on mitochondrial dysfunctioning and inflammation in epileptogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Increased Amyloidogenic Neuronal Injury in HIV-1-infected APP-KI Alzheimer's disease mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Spermidine reduces peri-implant inflammation and fibrosis to nurture osseointegration.Bioactive materials · 2026Article
- Multiple sclerosis pathophysiology: a comprehensive review of genetic, environmental, and immunological drivers.Inflammopharmacology · 2025Review
- Disrupting the TRAF1/cIAP2 interaction attenuates inflammasome activation and protects against monosodium urate crystal-induced arthritis.ImmunoHorizons · 2025Article
- Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- MYSM1 promotes lung adenocarcinoma progression via TRAF2/3-mediated activation of MAPK and non-canonical NF-κB pathways.NPJ precision oncology · 2025Article
- Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency.Blood cancer discovery · 2025Article
- Connectivity and Adaptation Patterns of the Deep-Sea Ground-Forming Sponge Geodia hentscheli Across Its Entire Distribution.Molecular biology and evolution · 2025Article
- The archaeal classmBio · 2025Article
- Repeated Low-Level Inflammatory Challenge Leads to Alterations in the TNF-CXCL10 Signalling Pathway in Mouse Cerebral Endothelial Cells In Vitro.Journal of neurochemistry · 2025Article
- ImmunoMet Oncogenesis: A New Concept to Understand the Molecular Drivers of Cancer.Journal of clinical medicine · 2025Review
- Identification and characterization of cell niches in tissue from spatial omics data at single-cell resolution.Nature communications · 2025Article
- ZIKV induces P62-mediated autophagic degradation of TRAF6 through TRAF6-NS1 interaction.iScience · 2024Article
- Transport of Non-Steroidal Anti-Inflammatory Drugs across an Oral Mucosa Epithelium In Vitro Model.Pharmaceutics · 2024Article
- Inhibition of S6K lowers age-related inflammation and increases lifespan through the endolysosomal system.Nature aging · 2024Article
- Pathological progression of osteoarthritis: a perspective on subchondral bone.Frontiers of medicine · 2024Review
- Structural Characterization of TRAF6 N-Terminal for Therapeutic Uses and Computational Studies on New Derivatives.Pharmaceuticals (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewThis review presents an overview of the current knowledge of TRAF molecules in inflammation with an emphasis on available human evidence and direct RECENT
findingsThe tumor necrosis factor receptor (TNF-R)-associated factor (TRAF) family of cytoplasmic proteins was initially identified as signaling adaptors that bind directly to the intracellular domains of receptors of the TNF-R superfamily. It is now appreciated that TRAF molecules are widely employed in signaling by a variety of adaptive and innate immune receptors as well as cytokine receptors. TRAF-dependent signaling pathways typically lead to the activation of nuclear factor-κBs (NF-κBs), mitogen-activated protein kinases (MAPKs), or interferon-regulatory factors (IRFs). Most of these signaling pathways have been linked to inflammation, and therefore TRAF molecules were expected to regulate inflammation and inflammatory responses since their discovery in 1990s. However, direct SUMMARY: Increasing evidence indicates that TRAF molecules are versatile and indispensable regulators of inflammation and inflammatory responses and that aberrant expression or function of TRAFs contributes to the pathogenesis of inflammatory diseases.
Indexed as
Identifiers
What Socratic 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 Socratic graph.