ArticlePLoS biology2023
Rab26 restricts insulin secretion via sequestering Synaptotagmin-1.
Article in PLoS biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Calcium Nanoliposome Improves Glycemic Control in a Mouse Diabetes Mellitus Model.Pharmaceutical nanotechnology · 2026Article
- Rab26 promotes hypoxia-induced hyperproliferation of PASMCs by modulating the AT1R-STAT3-YAP axis.Cellular and molecular life sciences : CMLS · 2025Article
- METRNL represses beta-to-alpha cell trans-differentiation to maintain beta cell function under diabetic metabolic stress in mice.Diabetologia · 2025Article
- Deficiency of Rab26 causes behavioral defects in mice through impaired trafficking of serotonin (5-HT) transporter.iScience · 2025Article
- Rab27a regulates the transport of influenza virus membrane proteins to the plasma membrane.Nature communications · 2025Article
- The significance of calcium ions in cerebral ischemia-reperfusion injury: mechanisms and intervention strategies.Frontiers in molecular biosciences · 2025Review
- Bioinformatics Analysis and Experimental Validation for Exploring Key Molecular Markers for Glioblastoma.Applied biochemistry and biotechnology · 2024Article
- Inhibition of mTOR prevents glucotoxicity-mediated increase of SA-beta-gal, p16Biogerontology · 2024Article
- Article
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rab26 is known to regulate multiple membrane trafficking events, but its role in insulin secretion in pancreatic β cells remains unclear despite it was first identified in the pancreas. In this study, we generated Rab26-/- mice through CRISPR/Cas9 technique. Surprisingly, insulin levels in the blood of the Rab26-/- mice do not decrease upon glucose stimulation but conversely increase. Deficiency of Rab26 promotes insulin secretion, which was independently verified by Rab26 knockdown in pancreatic insulinoma cells. Conversely, overexpression of Rab26 suppresses insulin secretion in both insulinoma cell lines and isolated mouse islets. Islets overexpressing Rab26, upon transplantation, also failed to restore glucose homeostasis in type 1 diabetic mice. Immunofluorescence microscopy revealed that overexpression of Rab26 results in clustering of insulin granules. GST-pulldown experiments reveal that Rab26 interacts with synaptotagmin-1 (Syt1) through directly binding to its C2A domain, which interfering with the interaction between Syt1 and SNAP25, and consequently inhibiting the exocytosis of newcomer insulin granules revealed by TIRF microscopy. Our results suggest that Rab26 serves as a negative regulator of insulin secretion, via suppressing insulin granule fusion with plasma membrane through sequestering Syt1.
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What Socratic holds
Registered trials
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 Socratic graph.