ArticleBMB reports2024
Cereblon regulates the production of hepatic fibroblast growth factor 23 in diabetes.
Article in BMB reports, 2024. 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
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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.
- Cereblon enhances hepatic hepcidin production through estrogen-related receptor gamma activation.BMB reports · 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cereblon (CRBN) is an extensively expressed protein involved in crucial physiological processes. This study reveals CRBN's role in governing hepatic fibroblast growth factor 23 (FGF23) expression and production via the cyclic adenosine monophosphate (cAMP) pathway in diabetic conditions. The expressions of hepatic Crbn, Yin Yang 1 (Yy1), and Fgf23 genes were significantly increased in diabetic mice and forskolin (FSK)-treated primary hepatocytes, correlating with elevated FGF23 production. Overexpression of Crbn and Yy1 increased hepatic FGF23 and cytokines by upregulating YY1 gene expression, which was reduced in Crbn- and Yy1-silenced mice and primary hepatocytes. Besides, we also found that CRBN-mediated regulation of hepatic FGF23 involved YY1 recruitment to the Fgf23 gene promoters, evidenced by reporter assays, deletion studies, and mutant analyses. These findings identify CRBN and YY1 as key contributors to gluconeogenic signaling-driven FGF23 production and inflammation in diabetes, highlighting their potential as therapeutic targets for addressing metabolic disorders like diabetes. [BMB Reports 2024; 57(12): 533-538].
Indexed as
Identifiers
39384178PMC11693598What Socratic 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 Socratic graph.