ArticleAmerican journal of physiology. Endocrinology and metabolism2017
Menin and PRMT5 suppress GLP1 receptor transcript and PKA-mediated phosphorylation of FOXO1 and CREB.
Article in American journal of physiology. Endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Protein arginine methyltransferases as metabolic regulators: many roles beyond cancer.Science China. Life sciences · 2026Review
- Role of exercise in cardiovascular health: a narrative review from prevention to therapeutic utilizations.Frontiers in cardiovascular medicine · 2026Review
- Epigenetic Regulation of Pancreas Development and Function.Advances in anatomy, embryology, and cell biology · 2024Review
- Risk Stratification of Pancreatic Neuroendocrine Neoplasms Based on Clinical, Pathological, and Molecular Characteristics.Journal of clinical medicine · 2022Review
- Modeling MEN1 with Patient-Origin iPSCs Reveals GLP-1R Mediated Hypersecretion of Insulin.Cells · 2022Article
- Molecular study of the proliferation process of beta cells derived from pluripotent stem cells.Molecular biology reports · 2022Review
- Tandem mass tag-based proteomic profiling revealed potential therapeutic targets and mechanisms of liraglutide for the treatment of impaired glucose tolerance.Frontiers in endocrinology · 2022Article
- Article
- The Structure and Functions of PRMT5 in Human Diseases.Life (Basel, Switzerland) · 2021Review
- Review
- Liraglutide protects palmitate-induced INS-1 cell injury by enhancing autophagy mediated via FoxO1.Molecular medicine reports · 2021Article
- Protein Arginine Methyltransferase 5 FunctionsFrontiers in cell and developmental biology · 2021Article
- Mitogen Synergy: An Emerging Route to Boosting Human Beta Cell Proliferation.Frontiers in cell and developmental biology · 2021Review
- Article
- PRMT5 promotes epithelial-mesenchymal transition via EGFR-β-catenin axis in pancreatic cancer cells.Journal of cellular and molecular medicine · 2020Article
- GLP-1 signaling suppresses menin's transcriptional block by phosphorylation in β cells.The Journal of cell biology · 2019Article
- Menin Upregulates FOXO1 Protein Stability by Repressing Skp2-Mediated Degradation in β Cells.Pancreas · 2019Article
- MENIN loss as a tissue-specific driver of tumorigenesis.Molecular and cellular endocrinology · 2018Review
- Epigenetic regulation by the menin pathway.Endocrine-related cancer · 2017Review
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 at 2 institutions in 1 country.
Funding
Abstract
Menin is a scaffold protein that interacts with several epigenetic mediators to regulate gene transcription, and suppresses pancreatic β-cell proliferation. Tamoxifen-inducible deletion of multiple endocrine neoplasia type 1 (
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.