ArticleNature communications2022
Plasma membrane flipping of Syntaxin-2 regulates its inhibitory action on insulin granule exocytosis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- A role for theMolecular biology of the cell · 2026Article
- MicroRNA-Driven Regulation of β-Cell Function in Type 2 Diabetes: Molecular Mechanisms, Network Insights, and Translational Perspectives.Acta physiologica (Oxford, England) · 2026Review
- Membrane Protein Insertion in Cells: Principles, Pathways, and Quality Control.Chemical reviews · 2026Review
- EWAS in a polyphenol dense, DNA methylation-targeted, controlled diet and lifestyle study.Frontiers in nutrition · 2026Article
- Role of complexin 2 in the regulation of hormone secretion from the islet of Langerhans.American journal of physiology. Endocrinology and metabolism · 2025Article
- A role for thebioRxiv : the preprint server for biology · 2025Article
- Syntaxin-2 balances phagocytic uptake and phagolysosomal clearance in macrophages.Journal of cell science · 2025Article
- KATP Channels as Target for Remodeling Connectivity in Type 2 Diabetes.Function (Oxford, England) · 2025Article
- Septin5 deletion enhances β-cell exocytosis by releasing microtubule-tethered insulin granules onto plasma membrane.Nature communications · 2025Article
- Secretion of endoplasmic reticulum protein VAPB/ALS8 requires topological inversion.Nature communications · 2024Article
- Chronic Epinephrine-Induced Endoplasmic Reticulum and Oxidative Stress Impairs Pancreatic β-Cells Function and Fate.International journal of molecular sciences · 2024Article
- BRSK2 in pancreatic β cells promotes hyperinsulinemia-coupled insulin resistance and its genetic variants are associated with human type 2 diabetes.Journal of molecular cell biology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Enhancing pancreatic β-cell secretion is a primary therapeutic target for type-2 diabetes (T2D). Syntaxin-2 (Stx2) has just been identified to be an inhibitory SNARE for insulin granule exocytosis, holding potential as a treatment for T2D, yet its molecular underpinnings remain unclear. We show that excessive Stx2 recruitment to raft-like granule docking sites at higher binding affinity than pro-fusion syntaxin-1A effectively competes for and inhibits fusogenic SNARE machineries. Depletion of Stx2 in human β-cells improves insulin secretion by enhancing trans-SNARE complex assembly and cis-SNARE disassembly. Using a genetically-encoded reporter, glucose stimulation is shown to induce Stx2 flipping across the plasma membrane, which relieves its suppression of cytoplasmic fusogenic SNARE complexes to promote insulin secretion. Targeting the flipping efficiency of Stx2 profoundly modulates secretion, which could restore the impaired insulin secretion in diabetes. Here, we show that Stx2 acts to assist this precise tuning of insulin secretion in β-cells, including in diabetes.
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