ArticleProceedings of the National Academy of Sciences of the United States of America2026
A teleost-specific oxygen-immunity axis where FIH activates NF-κB via competitive IκBα binding.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Global warming-induced aquatic deoxygenation poses a severe physiological challenge to teleosts, often influencing their immune defense mechanisms. While aquatic organisms are under evolutionary pressure to balance metabolic adaptation with pathogen resistance, the molecular strategies they employ to overcome high pathogen loads under hypoxic stress remain poorly understood. Here, an oxygen-immunity regulatory axis was identified in teleosts, in which the oxygen sensor FIH (factor inhibiting HIF) activated the NF-κB pathway by competitively displacing p65 from IκBα. Experiments with FIH mutants showed that NF-κB activation did not require FIH hydroxylase activity. In vitro, FIH bound IκBα, promoted p65 nuclear translocation, and increased inflammatory gene expression. FIH knockdown blunted these responses. In vivo, CRISPR/Cas9-generated
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.