ArticleMolecular and cellular endocrinology2025
The interplay between FOXO1 and glucocorticoid signaling in promoting the terminal differentiation of somatotropes.
Article in Molecular and cellular endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Consensus Pituitary Atlas, a scalable resource for annotation, novel marker discovery, and analyses in mouse pituitary gland research.Cell reports · 2026Article
- NR3C1 is required for normal somatotrope differentiation and Foxo1 expression in pituitary.Endocrinology · 2026Article
- ScRNAseq Analysis of Chicken Embryonic Pituitary Reveals Cell Heterogeneity and a Cell Type Coexpressing Gh and Pomc.Endocrinology · 2025Article
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
Glucocorticoids play a pivotal role in terminal differentiation of pituitary somatotropes. However, the mechanisms for this remain poorly understood. Here we demonstrate that loss of the forkhead transcription factor, FOXO1, severely impairs glucocorticoid-induced expression of the gene encoding growth hormone (Gh1) both in vitro and in vivo. The mechanism appears to involve glucocorticoid induction of Foxo1 expression, nuclear localization, and increased binding associated with the Gh1 gene. An additional mechanism includes stabilization of the glucocorticoid receptor, NR3C1, possibly through FOXO1 induction of the chaperone protein, HSP90. Together these data suggest that glucocorticoid signaling and FOXO1 cooperate to promote Gh1 expression, an essential aspect of somatotrope terminal differentiation.
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.