ArticleBiology direct2026
EYA1 regulates CIITA phosphorylation to promote EYA1-CIITA-Runx2 complex formation and extracellular matrix integrity in osteoarthritis.
Article in Biology direct, 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
7 authors.
Funding
Abstract
backgroundOsteoarthritis (OA) involves progressive extracellular matrix (ECM) degradation in articular cartilage. We previously revealed that the m
methodsOA was induced in mice via injection of sodium monoiodoacetate (MIA). The histological architecture and proteoglycan content of the articular cartilage were evaluated using H&E and Safranin O-Fast Green staining, while subchondral bone microarchitecture was assessed by micro-computed tomography. Circulating proinflammatory cytokine levels were determined by ELISA.
resultsImmunoprecipitation and mass spectrometry analyses of articular cartilage from MIA-induced OA mice identified the transcriptional coactivator EYA1 (Eyes Absent Homolog 1) and CIITA (Class II Major Histocompatibility Complex Transactivator) as novel Runx2-interacting proteins. In vitro and in vivo experiments demonstrated that EYA1, CIITA, and Runx2 form a functional EYA1-CIITA-Runx2 complex that binds to the promoters of MMP and ADAMTS genes and activates their expression. Silencing any member of the complex significantly reduced transcription of these matrix-degrading enzymes. Furthermore, we identified EYA1 as a phosphatase that dephosphorylates CIITA at serine 782, a phosphorylation site targeted by Pim3 (provirus integration site for Moloney murine leukemia virus 3) under inflammatory conditions.
conclusionOur findings uncover a previously unrecognized transcriptional mechanism in OA pathogenesis, in which EYA1 promotes ECM degradation by regulating CIITA dephosphorylation and assembling a transcriptional complex with CIITA and Runx2. Targeting this pathway may provide a promising therapeutic strategy for OA.
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.