ArticleProceedings of the National Academy of Sciences of the United States of America2005
The dense core transmembrane vesicle protein IA-2 is a regulator of vesicle number and insulin secretion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 68 citations in OpenAlex.
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- Role of Receptor Protein Tyrosine Phosphatases (RPTPs) in Insulin Signaling and Secretion.International journal of molecular sciences · 2021Review
- Regenerative neurogenic response from glia requires insulin-driven neuron-glia communication.eLife · 2021Article
- Modulation of large dense core vesicle insulin content mediates rhythmic hormone release from pancreatic beta cells over the 24h cycle.PloS one · 2018Article
- Article
- Pathophysiologic changes in IA-2/IA-2β null mice are secondary to alterations in the secretion of hormones and neurotransmitters.Acta diabetologica · 2016Article
- The Ia-2β intronic miRNA, miR-153, is a negative regulator of insulin and dopamine secretion through its effect on the Cacna1c gene in mice.Diabetologia · 2015Article
- The minimal promoter region of the dense-core vesicle protein IA-2: transcriptional regulation by CREB.Acta diabetologica · 2015Article
- Aged insulin granules display reduced microtubule-dependent mobility and are disposed within actin-positive multigranular bodies.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The dense core vesicle protein IA-2, but not IA-2β, is required for active avoidance learning.Neuroscience · 2014Article
- Human fibrocytes express multiple antigens associated with autoimmune endocrine diseases.The Journal of clinical endocrinology and metabolism · 2014Article
- Insight into insulin secretion from transcriptome and genetic analysis of insulin-producing cells of Drosophila.Genetics · 2014Article
- Disruption of gene expression rhythms in mice lacking secretory vesicle proteins IA-2 and IA-2β.American journal of physiology. Endocrinology and metabolism · 2012Article
- Receptor type protein tyrosine phosphatases (RPTPs) - roles in signal transduction and human disease.Journal of cell communication and signaling · 2012Article
- Neonatal β cell development in mice and humans is regulated by calcineurin/NFAT.Developmental cell · 2012Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
IA-2 is an enzymatically inactive member of the transmembrane protein tyrosine phosphate family located in dense core secretory vesicles and a major autoantigen in type 1 diabetes. Recent studies showed that targeted disruption of the IA-2 gene in mice resulted in impairment of insulin secretion and glucose intolerance. Insulin homeostasis, however, is a complex process involving a cascade of regulatory factors, and IA-2 is widely expressed in neuroendocrine cells throughout the body. Consequently, it is uncertain whether the impairment of insulin secretion in IA-2 knockout mice is a direct result of the knockout of IA-2 in beta cells or to counter regulatory alterations resulting from IA-2 knockout in other neuroendocrine cells. To define the function of IA-2, we studied the secretion of insulin in a single cell type, MIN-6, by overexpressing and knocking down IA-2. Our experiments showed that overexpression of IA-2 resulted in a 6-fold increase in glucose- or K+-induced insulin secretion and a approximately 3-fold increase in the number of secretory vesicles and the insulin content of cells. In contrast, knockdown of endogenous IA-2 by short interfering RNA resulted in nearly a complete loss of glucose-induced insulin secretion and a 50% decrease in basal insulin release. The half-life of insulin in cells overexpressing IA-2 was nearly twice as great as that in mock-transfected cells, suggesting that IA-2 was stabilizing the insulin-containing vesicles. From these results we conclude that in beta cells, IA-2 is an important regulator of dense core vesicle number and glucose-induced and basal insulin secretion.
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