ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
N-terminal insertion and C-terminal ankyrin-like repeats of alpha-latrotoxin are critical for Ca2+-dependent exocytosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- The Dissociation of Latrophilin Fragments by Perfluorooctanoic Acid (PFOA) Inhibits LTXToxins · 2025Article
- Structural basis of α-latrotoxin transition to a cation-selective pore.Nature communications · 2024Article
- Article
- Human antibodies neutralizing the alpha-latrotoxin of the European black widow.Frontiers in immunology · 2024Article
- Conformational states of syntaxin-1 govern the necessity of N-peptide binding in exocytosis of PC12 cells and Caenorhabditis elegans.Molecular biology of the cell · 2016Article
- Calcium-dependent activator protein for secretion 1 (CAPS1) binds to syntaxin-1 in a distinct mode from Munc13-1.The Journal of biological chemistry · 2013Article
- Article
- High yield derivation of enriched glutamatergic neurons from suspension-cultured mouse ESCs for neurotoxicology research.BMC neuroscience · 2012Article
- A novel evolutionarily conserved domain of cell-adhesion GPCRs mediates autoproteolysis.The EMBO journal · 2012Article
- Alpha-latrotoxin rescues SNAP-25 from BoNT/A-mediated proteolysis in embryonic stem cell-derived neurons.Toxins · 2011Article
- Penelope's web: using alpha-latrotoxin to untangle the mysteries of exocytosis.Journal of neurochemistry · 2009Review
- Alpha-latrotoxin stimulates a novel pathway of Ca2+-dependent synaptic exocytosis independent of the classical synaptic fusion machinery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Munc18-1 is critical for plasma membrane localization of syntaxin1 but not of SNAP-25 in PC12 cells.Molecular biology of the cell · 2008Article
- alpha-Latrotoxin and its receptors.Handbook of experimental pharmacology · 2008Review
- Insecticidal toxins from black widow spider venom.Toxicon : official journal of the International Society on Toxinology · 2007Review
- RalA and RalB function as the critical GTP sensors for GTP-dependent exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Crystal structure of the second LNS/LG domain from neurexin 1alpha: Ca2+ binding and the effects of alternative splicing.The Journal of biological chemistry · 2006Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alpha-latrotoxin, a potent stimulator of exocytosis from neurons and neuroendocrine cells, has been studied intensively, but the mechanisms of its actions are poorly understood. Here, we developed a new method to generate active recombinant alpha-latrotoxin and conducted a structure/function analysis of the toxin in stimulating Ca2+-dependent exocytosis. alpha-Latrotoxin consists of a conserved N-terminal domain and C-terminal ankyrin-like repeats. After cleavage of an N-terminally fused purification tag of glutathione S-transferase (GST), the recombinant toxin strongly stimulated exocytosis, whereas the GST-fused toxin was much less potent. The GST-fused toxin bound to the receptors [neurexin 1alpha; CL1 (CIRL/latrophilin 1)] as efficiently as did the GST-cleaved toxin but was much less effective in inserting into the plasma membrane and inducing cation conductance. The toxin with deletion of the last two ankyrin-like repeats still bound the receptors but could neither stimulate exocytosis nor induce cation conductance efficiently. The abilities of the mutated toxins to stimulate exocytosis correlated well with their abilities to induce cation conductance, but not their binding to the receptors. Our results indicate that (1) C-terminal ankyrin-like repeats and a free (unfused) N terminus are both required for the toxin to form pores, which is essential for Ca2+-dependent exocytosis, and (2) receptor binding alone is not sufficient to stimulate Ca2+-dependent exocytosis.
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