ArticleCellular and molecular life sciences : CMLS2018
BRD7 regulates the insulin-signaling pathway by increasing phosphorylation of GSK3β.
Article in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 18 citations in OpenAlex.
- Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation.Cellular and molecular gastroenterology and hepatology · 2026Article
- Zinc and Type 2 Diabetes: A Systematic Review with a Narrative Synthesis of Their Bidirectional Relationship and Clinical Perspectives for Personalized Nutritional Support.Diseases (Basel, Switzerland) · 2025Review
- BRD7 facilitates ferroptosis via modulating clusterin promoter hypermethylation and suppressing AMPK signaling in diabetes-induced testicular damage.Molecular medicine (Cambridge, Mass.) · 2024Article
- Proteome Analysis Related to Unsaturated Fatty Acid Synthesis by Interfering with Bovine AdipocyteAntioxidants (Basel, Switzerland) · 2024Article
- BRD7 improves glucose homeostasis independent of IRS proteins.The Journal of endocrinology · 2023Article
- New insights into the role of GSK-3β in the brain: from neurodegenerative disease to tumorigenesis.PeerJ · 2023Review
- The regulatory subunits of PI3K, p85α and p85β, differentially affect BRD7-mediated regulation of insulin signaling.Journal of molecular cell biology · 2022Article
- O-GlcNAcylation in Hyperglycemic Pregnancies: Impact on Placental Function.Frontiers in endocrinology · 2021Review
- Emerging Roles of BRD7 in Pathophysiology.International journal of molecular sciences · 2020Review
- A Critical Review of Proteomic Studies in Gestational Diabetes Mellitus.Journal of diabetes research · 2020Review
- BRD7 deficiency leads to the development of obesity and hyperglycemia.Scientific reports · 2019Article
- Bromodomain‑containing protein 7 sensitizes breast cancer cells to paclitaxel by activating Bcl2‑antagonist/killer protein.Oncology reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Reduced hepatic expression levels of bromodomain-containing protein 7 (BRD7) have been suggested to play a role in the development of glucose intolerance in obesity. However, the molecular mechanism by which BRD7 regulates glucose metabolism has remained unclear. Here, we show that BRD7 increases phosphorylation of glycogen synthase kinase 3β (GSK3β) in response to activation of the insulin receptor-signaling pathway shortly after insulin stimulation and the nutrient-sensing pathway after feeding. BRD7 mediates phosphorylation of GSK3β at the Serine 9 residue and this effect on GSK3β occurs even in the absence of AKT activity. Using both in vitro and in vivo models, we further demonstrate that BRD7 mediates phosphorylation of ribosomal protein S6 kinase (S6K) and leads to increased phosphorylation of the eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) and, therefore, relieves its inhibition of the eukaryotic translation initiation factor 4E (eIF4E). However, the increase in phosphorylation of 4E-BP1 with BRD7 overexpression is blunted in the absence of AKT activity. In addition, using liver-specific BRD7 knockout (LBKO) mice, we show that BRD7 is required for mTORC1 activity on its downstream molecules. These findings show a novel basis for understanding the molecular dynamics of glucose metabolism and suggest the unique function of BRD7 in the regulation of glucose homeostasis.
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.