ArticlePloS one2019
Expression of mutant mRNA and protein in pancreatic cells derived from MODY3- iPS cells.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Patient-derived induced pluripotent stem cells for precision modelling of monogenic beta cell disorders.Frontiers in endocrinology · 2026Review
- Integrative single-cell multi-omics profiling of human pancreatic islets identifies T1D-associated genes and regulatory signals.Cell reports · 2025Article
- Towards a better understanding of diabetes mellitus using organoid models.Nature reviews. Endocrinology · 2023Review
- A Potential Therapy Using Antisense Oligonucleotides to Treat Autosomal Recessive Polycystic Kidney Disease.Journal of clinical medicine · 2023Article
- Derivation and characteristics of induced pluripotent stem cells from a patient with acute myelitis.Frontiers in cell and developmental biology · 2023Article
- HNF1A Mutations and Beta Cell Dysfunction in Diabetes.International journal of molecular sciences · 2022Review
- An HNF1α truncation associated with maturity-onset diabetes of the young impairs pancreatic progenitor differentiation by antagonizing HNF1β function.Cell reports · 2022Article
- Stem Cell-Derived β Cells: A Versatile Research Platform to Interrogate the Genetic Basis of β Cell Dysfunction.International journal of molecular sciences · 2022Review
- Modeling different types of diabetes using human pluripotent stem cells.Cellular and molecular life sciences : CMLS · 2021Review
- Genome Editing Human Pluripotent Stem Cells to Model β-Cell Disease and Unmask Novel Genetic Modifiers.Frontiers in endocrinology · 2021Review
- Modeling Maturity Onset Diabetes of the Young in Pluripotent Stem Cells: Challenges and Achievements.Frontiers in endocrinology · 2021Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maturity-onset diabetes of the young (MODY) is a heterozygous monogenic diabetes; more than 14 disease genes have been identified. However, the pathogenesis of MODY is not fully understood because the patients' pancreatic beta cells are inaccessible. To elucidate the pathology of MODY, we established MODY3 patient-derived iPS (MODY3-iPS) cells using non-integrating Sendai virus (SeV) vector and examined the mutant mRNA and protein of HNF1A (Hepatocyte Nuclear factor 1A) after pancreatic lineage differentiation. Our patient had a cytosine insertion in the HNF1A gene (P291fsinsC) causing frameshift and making a premature termination codon (PTC). We confirmed these MODY3-iPS cells possessed the characteristics of pluripotent stem cells. After we differentiated them into pancreatic beta cells, transcripts of HNF1A gene were cloned and sequenced. We found that P291fsinsC mutant transcripts were much less frequent than wild ones, but they increased after adding cycloheximide (CHX) to the medium. These results suggested that mutant mRNA was destroyed by nonsense-mediated mRNA decay (NMD). Moreover, we were not able to detect any band of mutant proteins in pancreatic lineage cells which were differentiated from MODY3-iPSCs by western blot (WB) analysis. A scarcity of the truncated form of mutant protein may indicate that MODY3 might be caused by a haplo-insufficiency effect rather than a dominant negative manner.
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