ArticleCellular & molecular immunology2026
MDA5 regulates BCR signaling and B-cell function via NF-κB-mediated DNM1.
Article in Cellular & molecular immunology, 2026. 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
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
2 citing papers in PubMed.
- Development and validation of a novel prognostic and for osteosarcoma patients utilizing multiple organelle related genes.Discover oncology · 2026Article
- Structural and functional perspectives on DEAD-box RNA helicases in the rubber tree cold stress response.Frontiers in plant science · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
32 authors.
Funding
Abstract
Melanoma Differentiation-Associated gene 5 (MDA5) serves as a pattern recognition receptor (PRR) that identifies pathogen-associated molecular patterns (PAMPs), making it instrumental in antiviral defense. However, its non-canonical role in adaptive immunity, particularly in regulating B-cell immune functions, is poorly characterized. Here, we demonstrate that MDA5 is critical for the marginal zone (MZ) B-cell differentiation, B-cell receptor (BCR) signal transduction, and cytoskeletal dynamics. We determined that the MDA5-NF-κB-DNM1 axis governs actin polymerization and that this impairment in Mda5 knockout (KO) B cells can be rescued by the treatment with the dynamin1 (DNM1) activator Bis-T-23. Furthermore, MDA5 deficiency induces metabolic perturbations in B cells, characterized by a reduced extracellular acidification rate (ECAR) and oxygen consumption rate (OCR), excessive reactive oxygen species (ROS) accumulation, and increased mitochondrial fission. Notably, taurine levels are decreased in Mda5 KO B cells, and in vitro taurine supplementation rescues impaired BCR signaling. Finally, MDA5-deficient mice exhibit a blunted humoral immune response. Overall, this study reveals the key functions and molecular mechanisms of MDA5 in B-cell differentiation, BCR signaling, and the humoral immune response.
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.