ArticleCell death & disease2016
Junctophilin 3 expresses in pancreatic beta cells and is required for glucose-stimulated insulin secretion.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Epigenome-wide association study of incident type 2 diabetes in Black and White participants from the Atherosclerosis Risk in Communities Study.Diabetologia · 2025Article
- Plasma membrane curvature regulates the formation of contacts with the endoplasmic reticulum.Nature cell biology · 2024Article
- Membrane Curvature Promotes ER-PM Contact Formation via Junctophilin-EHD Interactions.bioRxiv : the preprint server for biology · 2024Article
- Structure, Function, and Regulation of the Junctophilin Family.Annual review of physiology · 2024Review
- Relationship between DNA methylation changes and skeletal muscle mass.BMC genomic data · 2023Article
- Asiatic acid improves insulin secretion ofZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Article
- Insulin secretion deficits in a Prader-Willi syndrome β-cell model are associated with a concerted downregulation of multiple endoplasmic reticulum chaperones.PLoS genetics · 2023Article
- NMR resonance assignments of the DNA binding domain of mouse Junctophilin-2.Biomolecular NMR assignments · 2022Article
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- Structures of the junctophilin/voltage-gated calcium channel interface reveal hot spot for cardiomyopathy mutations.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Builders of the Junction: Roles of Junctophilin1 and Junctophilin2 in the Assembly of the Sarcoplasmic Reticulum-Plasma Membrane Junctions in Striated Muscle.Biomolecules · 2022Review
- Mitofusin2 PromotesStem cells international · 2022Article
- Neuronal junctophilins recruit specific CaeLife · 2021Article
- Junctophilins: Key Membrane Tethers in Muscles and Neurons.Frontiers in molecular neuroscience · 2021Review
- Nanoscale coupling of junctophilin-2 and ryanodine receptors regulates vascular smooth muscle cell contractility.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Article
- A junctophilin-caveolin interaction enables efficient coupling between ryanodine receptors and BKThe Journal of biological chemistry · 2019Article
- Molecular determinants of homo- and heteromeric interactions of Junctophilin-1 at triads in adult skeletal muscle fibers.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Article
- Integrated Bioinformatics Analysis of Master Regulators in Anaplastic Thyroid Carcinoma.BioMed research international · 2019Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well accepted that junctophilin (JPHs) isoforms act as a physical bridge linking plasma membrane and endoplasmic reticulum (ER) for channel crosstalk in excitable cells. Our purpose is to investigate whether JPHs are involved in the proper communication between Ca(2+) influx and subsequent Ca(2+) amplification in pancreatic beta cells, thereby participating in regulating insulin secretion. The expression of JPH isoforms was examined in human and mouse pancreatic tissues, and JPH3 expression was found in both the beta cells. In mice, knockdown of Jph3 (si-Jph3) in islets decreased glucose-stimulated insulin secretion (GSIS) accompanied by mitochondrial function impairment. Si-Jph3 lowered the insulin secretory response to Ca(2+) signaling in the presence of glucose, and reduced [Ca(2+)]c transient amplitude triggered by caffeine. Si-Jph3 also attenuated mitofusin 2 expression, thereby disturbing the spatial organization of ER-mitochondria contact in islets. These results suggest that the regulation of GSIS by the KATP channel-independent pathways is partly impaired due to decrease of JPH3 expression in mouse islets. JPH3 also binds to type 2 ryanodine receptors (RyR2) in mouse and human pancreatic tissues, which might contribute to Ca(2+) release amplification in GSIS. This study demonstrates some previously unrecognized findings in pancreatic tissues: (1) JPH3 expresses in mouse and human beta cells; (2) si-Jph3 in mouse primary islets impairs GSIS in vitro; (3) impairment in GSIS in si-Jph3 islets is due to changes in RyR2-[Ca(2+)]c transient amplitude and ER-mitochondria contact.
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