ArticleAdvanced biotechnology2026
EYA4 promotes cellular senescence by enhancing P21 transcription through interaction with SIX2.
Article in Advanced biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Immunoglobulin Superfamily Protein BTNL9 Functions as a Non-Canonical Transcriptional Regulator to Suppress NSCLC Through Cell Cycle and p53 Pathways.International journal of molecular sciences · 2026Article
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
During the aging process, the expression levels of numerous genes undergo significant changes, some of which in turn regulate the progression of aging. In this study, we identified the expression of EYA4 is upregulated during aging and demonstrated its critical role in modulating cellular senescence. Knockdown of EYA4 significantly delays both replicative and stress-induced cellular senescence. Mechanistic investigations showed that EYA4 interacts with the transcription factor SIX2 to promote the expression of p21, a key molecule in the senescence-signaling pathway, which accelerates cellular senescence. Interestingly, EYA4 possesses both transcriptional activation and phosphatase activities, yet experiments using phosphatase-deficient mutants revealed that its ability to enhance p21 expression is independent of its phosphatase activity. Further analysis demonstrated that the EYA4-SIX2-mediated regulation of p21 expression is p53-dependent, as the absence of p53 abolished this regulatory effect. In conclusion, our findings uncover a novel role of the EYA4-SIX2 complex in promoting cellular senescence through the transcriptional activation of p21. Targeting EYA4 may represent a promising strategy for delaying the aging process.
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.