ArticleExperimental diabetes research2010
Deletion of the Men1 gene prevents streptozotocin-induced hyperglycemia in mice.
Article in Experimental diabetes research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Menin-regulated Pbk controls high fat diet-induced compensatory beta cell proliferation.EMBO molecular medicine · 2021Article
- 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
- Overexpression of ST5, an activator of Ras, has no effect on β-cell proliferation in adult mice.Molecular metabolism · 2018Article
- Multiple Endocrine Neoplasia Syndromes from Genetic and Epigenetic Perspectives.Biomarker insights · 2018Review
- Epigenetic regulation by the menin pathway.Endocrine-related cancer · 2017Review
- Menin and PRMT5 suppress GLP1 receptor transcript and PKA-mediated phosphorylation of FOXO1 and CREB.American journal of physiology. Endocrinology and metabolism · 2017Article
- Menin: a scaffold protein that controls gene expression and cell signaling.Trends in biochemical sciences · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetes ultimately results from an inadequate number of functional beta cells in the islets of Langerhans. Enhancing proliferation of functional endogenous beta cells to treat diabetes remains underexplored. Here, we report that excision of the Men1 gene, whose loss-of-function mutation leads to inherited multiple endocrine neoplasia type 1 (MEN1), rendered resistant to streptozotocin-induced hyperglycemia in a tamoxifen-inducible and temporally controlled Men1 excision mouse model as well as in a tissue-specific Men1 excision mouse model. Men1 excision prevented mice from streptozotocin-induced hyperglycemia mainly through increasing the number of functional beta cells. BrdU incorporation by beta cells, islet size, and circulating insulin levels were significantly increased in Men1-excised mice. Membrane localization of glucose transporter 2 was largely preserved in Men1-excised beta cells, but not in Men1-expressing beta cells. Our findings suggest that repression of menin, a protein encoded by the Men1 gene, might be a valuable means to maintain or increase the number of functional endogenous beta cells to prevent or ameliorate diabetes.
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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.