ArticleDevelopment (Cambridge, England)2015
Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- A stem cell knockout village reveals lineage rewiring and a non-canonical islet cell fate in monogenic diabetes.bioRxiv : the preprint server for biology · 2025Article
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- MNX1 mutations causing neonatal diabetes: Review of the literature and report of a case with extra-pancreatic congenital defects presenting in severe diabetic ketoacidosis.Journal of diabetes investigation · 2023Review
- Mechanisms associated with t(7;12) acute myeloid leukaemia: from genetics to potential treatment targets.Bioscience reports · 2023Review
- Article
- Integrating single cell transcriptomics and volume electron microscopy confirms the presence of pancreatic acinar-like cells in sea urchins.Frontiers in cell and developmental biology · 2022Article
- Bioinformatics network analyses of growth differentiation factor 11.Open life sciences · 2022Article
- Conversion of Gastrointestinal Somatostatin-Expressing D Cells Into Insulin-Producing Beta-Like Cells UponFrontiers in endocrinology · 2022Article
- Sex-biased islet β cell dysfunction is caused by the MODY MAFA S64F variant by inducing premature aging and senescence in males.Cell reports · 2021Article
- Do second generation sequencing techniques identify documented genetic markers for neonatal diabetes mellitus?Heliyon · 2021Review
- Sequential progenitor states mark the generation of pancreatic endocrine lineages in mice and humans.Cell research · 2021Article
- Retinoic acid signaling within pancreatic endocrine progenitors regulates mouse and human β cell specification.Development (Cambridge, England) · 2020Article
- Article
- Myt Transcription Factors Prevent Stress-Response Gene Overactivation to Enable Postnatal Pancreatic β Cell Proliferation, Function, and Survival.Developmental cell · 2020Article
- Article
- Point mutations in the PDX1 transactivation domain impair human β-cell development and function.Molecular metabolism · 2019Article
- Transgene-associated human growth hormone expression in pancreatic β-cells impairs identification of sex-based gene expression differences.American journal of physiology. Endocrinology and metabolism · 2019Article
- Islets from human donors with higher but not lower hemoglobin A1c levels respond to gastrin treatment in vitro.PloS one · 2019Article
- Functional Defects From Endocrine Disease-Associated Mutations in HLXB9 and Its Interacting Partner, NONO.Endocrinology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Homozygous Mnx1 mutation causes permanent neonatal diabetes in humans, but via unknown mechanisms. Our systematic and longitudinal analysis of Mnx1 function during murine pancreas organogenesis and into the adult uncovered novel stage-specific roles for Mnx1 in endocrine lineage allocation and β-cell fate maintenance. Inactivation in the endocrine-progenitor stage shows that Mnx1 promotes β-cell while suppressing δ-cell differentiation programs, and is crucial for postnatal β-cell fate maintenance. Inactivating Mnx1 in embryonic β-cells (Mnx1(Δbeta)) caused β-to-δ-like cell transdifferentiation, which was delayed until postnatal stages. In the latter context, β-cells escaping Mnx1 inactivation unexpectedly upregulated Mnx1 expression and underwent an age-independent persistent proliferation. Escaper β-cells restored, but then eventually surpassed, the normal pancreatic β-cell mass, leading to islet hyperplasia in aged mice. In vitro analysis of islets isolated from Mnx1(Δbeta) mice showed higher insulin secretory activity and greater insulin mRNA content than in wild-type islets. Mnx1(Δbeta) mice also showed a much faster return to euglycemia after β-cell ablation, suggesting that the new β-cells derived from the escaper population are functional. Our findings identify Mnx1 as an important factor in β-cell differentiation and proliferation, with the potential for targeting to increase the number of endogenous β-cells for diabetes therapy.
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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.