ArticleDiabetes2025
IER3IP1 Mutations Cause Neonatal Diabetes Due to Impaired Proinsulin Trafficking.
Article in Diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Ghrelin and relamorelin counteract hypoglycemia in mice engrafted with congenital hyperinsulinism stem cell-derived islets.Stem cells translational medicine · 2026Article
- Article
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
- Microcephaly, Epilepsy, and Diabetes Syndrome 1: A Moroccan Case Report of Novel Compound HeterozygousBalkan journal of medical genetics : BJMG · 2025Article
- Article
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13 authors.
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Abstract
article highlightsIER3IP1 mutations are linked to the development of microcephaly, epilepsy, and early-onset diabetes syndrome 1. However, the underlying molecular mechanisms of cell dysfunction are unknown. Using targeted genome editing, we generated specific IER3IP1 mutations in human embryonic stem cell lines that were differentiated into pancreatic islet lineages. Loss of IER3IP1 resulted in a threefold reduction in endoplasmic reticulum-to-Golgi trafficking of proinsulin in stem cell-derived β-cells, leading to β-cell dysfunction both in vitro and in vivo. Loss of IER3IP1 also triggered increased markers of endoplasmic reticulum stress, indicating the pivotal role of the endoplasmic reticulum-to-Golgi trafficking pathway for β-cell homeostasis and function.
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