ArticleFrontiers in aging2025
EI24 binds to IGF1R, enhancing glucose homeostasis and fostering healthy aging in male mice.
Article in Frontiers in aging, 2025. 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The etoposide-induced 2.4 kb transcript (EI24) plays a crucial role in autophagy, facilitating the clearance of damaged proteins and organelles to maintain cellular homeostasis. While autophagy is widely recognized for its beneficial effects on healthy aging, the effects of EI24 overexpression remain unclear. Methods: We analyzed the interaction of EI24 with the insulin-like growth factor 1 receptor (IGF1R), a key molecule associated with aging. Results: EI24 was found to bind to IGF1R, specifically engaging with its transmembrane (TM) domain near the cytoplasmic membrane, and suppress its phosphorylation. Male Conclusion: These findings suggest that Ei24 overexpression contributes to improved glucose regulation and healthier aging across multiple organs. By interacting with IGF1R, EI24 may provide a novel mechanism for promoting metabolic and age-related health.
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.