ArticleThe EMBO journal1998
Ca2+-independent insulin exocytosis induced by alpha-latrotoxin requires latrophilin, a G protein-coupled receptor.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 83 citations in OpenAlex.
- Contribution of metabolism-independent glucose sensing to metabolic homeostasis.Trends in endocrinology and metabolism: TEM · 2026Review
- The Role of G Protein-Coupled Receptors and Receptor Kinases in PancreaticPharmacological reviews · 2024Review
- ADGRL1 is a glucose receptor involved in mediating energy and glucose homeostasis.Diabetologia · 2024Article
- Skeletal muscle metabolism and contraction performance regulation by teneurin C-terminal-associated peptide-1.Frontiers in physiology · 2022Article
- Widow spiders in the New World: a review onThe journal of venomous animals and toxins including tropical diseases · 2021Article
- Insulin Release Mechanism Modulated by Toxins Isolated from Animal Venoms: From Basic Research to Drug Development Prospects.Molecules (Basel, Switzerland) · 2019Review
- Article
- Toxins that modulate ionic channels as tools for exploring insulin secretion.Cellular and molecular neurobiology · 2010Review
- Genome-wide association identifies candidate genes that influence the human electroencephalogram.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- The latrophilins, "split-personality" receptors.Advances in experimental medicine and biology · 2010Review
- Penelope's web: using alpha-latrotoxin to untangle the mysteries of exocytosis.Journal of neurochemistry · 2009Review
- Domain shuffling and the evolution of vertebrates.Genome research · 2009Article
- alpha-Latrotoxin and its receptors.Handbook of experimental pharmacology · 2008Review
- alpha-Latrotoxin increases spontaneous and depolarization-evoked exocytosis from pancreatic islet beta-cells.The Journal of physiology · 2005Article
- The alpha-latrotoxin mutant LTXN4C enhances spontaneous and evoked transmitter release in CA3 pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Sensitization of regulated exocytosis by protein kinase C.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- alpha-Latrotoxin releases calcium in frog motor nerve terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Inhibition of quantal release from motor nerve by wortmannin.British journal of pharmacology · 1999Article
- Norepinephrine exocytosis stimulated by alpha-latrotoxin requires both external and stored Ca2+ and is mediated by latrophilin, G proteins and phospholipase C.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 1999Review
- Black widow spider alpha-latrotoxin: a presynaptic neurotoxin that shares structural homology with the glucagon-like peptide-1 family of insulin secretagogic hormones.Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology · 1998Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
alpha-Latrotoxin (alpha-LTX) induces exocytosis of small synaptic vesicles (SSVs) in neuronal cells both by a calcium-independent mechanism and by opening cation-permeable pores. Since the basic molecular events regulating exocytosis in neurons and endocrine cells may be similar, we have used the exocytosis of insulin-containing large dense core vesicles (LDCVs) as a model system. In primary pancreatic beta-cells and in the derived cell lines INS-1 and MIN6, alpha-LTX increased insulin release in the absence of extracellular calcium, but the insulin-secreting cell lines HIT-T15 and RINm5F were unresponsive. alpha-LTX did not alter membrane potential or cytosolic calcium, and its stimulatory effect on exocytosis was still observed in pre-permeabilized INS-1 cells kept at 0.1 microM Ca2+. Consequently, pore formation or ion fluxes induced by alpha-LTX could be excluded. The Ca2+-independent alpha-LTX-binding protein, latrophilin, is a novel member of the secretin family of G protein-coupled receptors (GPCR). Sensitivity to alpha-LTX correlated with expression of latrophilin, but not with synaptotagmin I or neurexin Ialpha expression. Moreover, transient expression of latrophilin in HIT-T15 cells conferred alpha-LTX-induced exocytosis. Our results indicate that direct stimulation of exocytosis by a GPCR mediates the Ca2+-independent effects of alpha-LTX in the absence of altered ion fluxes. Therefore, direct regulation by receptor-activated heterotrimeric G proteins constitutes an important feature of the endocrine exocytosis of insulin-containing LDCVs and may also apply to SSV exocytosis in neurons.
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