ArticleJournal of virology2009
Identification of TRIM23 as a cofactor involved in the regulation of NF-kappaB by human cytomegalovirus.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- To TRIM the Immunity: From Innate to Adaptive Immunity.Frontiers in immunology · 2020Pooled it
- Exploiting Ubiquitination: African Swine Fever Virus-Mediated Recruitment of Host E3 Ligases During Viral Infection and Immune Regulation.Pathogens (Basel, Switzerland) · 2026Review
- TRIM proteins as emerging regulators of immune pathways: potential therapeutic targets in immune-related disorders.Frontiers in immunology · 2026Review
- A Transcriptomic Approach to Sex Differences in Calcific Aortic Valve Stenosis in Patients with a Tricuspid Aortic Valve.CJC open · 2025Article
- TRIM28 is an essential regulator of three-dimensional chromatin state underpinning CD8Nature communications · 2025Article
- Review
- TRIMming down Flavivirus Infections.Viruses · 2024Review
- Tripartite motif containing 23 functions as a critical regulator in macrophages to control the pathological feature of diabetic nephropathy.International urology and nephrology · 2023Article
- Deletion of the non-adjacent genesFrontiers in immunology · 2023Article
- Grouper TRIM23 exerts antiviral activity against iridovirus and nodavirus.Frontiers in immunology · 2022Article
- TRIMs: selective recruitment at different steps of the NF-κB pathway-determinant of activation or resolution of inflammation.Cellular and molecular life sciences : CMLS · 2021Review
- TRIMming Type I Interferon-Mediated Innate Immune Response in Antiviral and Antitumor Defense.Viruses · 2021Review
- MicroRNA-497 Reduction and Increase of Its Family Member MicroRNA-424 Lead to Dysregulation of Multiple Inflammation Related Genes in Synovial Fibroblasts With Rheumatoid Arthritis.Frontiers in immunology · 2021Article
- The Roles of TRIMs in Antiviral Innate Immune Signaling.Frontiers in cellular and infection microbiology · 2021Review
- Molecular characterisation, expression and functional feature of TRAF6 in the King pigeon (Innate immunity · 2020Article
- Where do we Stand after Decades of Studying Human Cytomegalovirus?Microorganisms · 2020Review
- Elevated TRIM23 expression predicts cisplatin resistance in lung adenocarcinoma.Cancer science · 2020Article
- TRIM Proteins in Host Defense and Viral Pathogenesis.Current clinical microbiology reports · 2020Review
- TRIM Proteins and Their Roles in Antiviral Host Defenses.Annual review of virology · 2018Review
- The Interplay between Human Cytomegalovirus and Pathogen Recognition Receptor Signaling.Viruses · 2018Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Human cytomegalovirus (HCMV) regulates NF-kappaB during infection by a variety of mechanisms. For example, the HCMV gene product, UL144, is known to activate NF-kappaB in a tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6)-dependent manner, causing the upregulation of the chemokine CCL22 (MDC). Viral UL144 is expressed from the UL/b' region of the HCMV genome at early times postinfection and is a TNFR1-like homologue. Despite this homology to the TNFR1 receptor superfamily, UL144 does not bind to members of the TNF ligand superfamily. We show here that the upregulation of NF-kappaB by UL144 is dependent upon cellular tripartite motif 23 (TRIM23) protein. We propose a mechanism by which UL144 activates NF-kappaB through a direct interaction with the cellular protein TRIM23 in a complex containing TRAF6. In contrast, TRIM23 is not involved in conventional double-stranded RNA signaling via NF-kappaB. Therefore, we present a novel role for TRIM23 that is specific to UL144-mediated activation of NF-kappaB during the course of virus infection.
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.