ArticleFrontiers in immunology2025
Fbxo16 mediates degradation of NF-κB p65 subunit and inhibits inflammatory response in dendritic cells.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- PDLIM2 acts as a central regulator of ubiquitination, immune signaling, and mitochondrial metabolism in lung cancer suppression (Review).International journal of oncology · 2026Review
- Development of a 5K Liquid-Phase Genome-Wide Breeding Chip for Xinglong Buffalo.Animals : an open access journal from MDPI · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of transcription factor NF-κB is tightly regulated by negative regulatory systems that prevent excessive inflammation leading to autoimmune diseases. We previously demonstrated that PDLIM2, a PDZ-LIM domain-containing nuclear protein, functions as a ubiquitin E3 ligase that targets the p65 subunit of NF-κB and STAT3/STAT4 transcription factors for proteasomal degradation, thus terminating immune responses in dendritic cells and CD4
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Registered trials
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