ArticleThe Journal of cell biology2019
GLP-1 signaling suppresses menin's transcriptional block by phosphorylation in β cells.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Extracellular signalling regulates gastrin transcription through site-specific phosphorylation and nuclear redistribution of Menin.bioRxiv : the preprint server for biology · 2026Article
- A neural substrate of comorbid depressive symptoms in alcohol use.Molecular psychiatry · 2025Article
- Exploring histone deacetylases in type 2 diabetes mellitus: pathophysiological insights and therapeutic avenues.Clinical epigenetics · 2024Review
- Menin Reduces Parvalbumin Expression and is Required for the Anti-Depressant Function of Ketamine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The potential of β-cell growth promotion, continued.Journal of diabetes · 2023Article
- Hypothalamic Menin regulates systemic aging and cognitive decline.PLoS biology · 2023Article
- Phosphorylation of 17β-hydroxysteroid dehydrogenase 13 at serine 33 attenuates nonalcoholic fatty liver disease in mice.Nature communications · 2022Article
- Modeling MEN1 with Patient-Origin iPSCs Reveals GLP-1R Mediated Hypersecretion of Insulin.Cells · 2022Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Both menin and glucagon-like peptide 1 (GLP-1) pathways play central yet opposing role in regulating β cell function, with menin suppressing, and GLP-1 promoting, β cell function. However, little is known as to whether or how GLP-1 pathway represses menin function. Here, we show that GLP-1 signaling-activated protein kinase A (PKA) directly phosphorylates menin at the serine 487 residue, relieving menin-mediated suppression of insulin expression and cell proliferation. Mechanistically, Ser487-phosphorylated menin gains increased binding affinity to nuclear actin/myosin IIa proteins and gets sequestrated from the
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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.