Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mutant alpha-latrotoxin (LTXN4C) does not form pores and causes secretion by receptor stimulation: this action does not require neurexins.

The Journal of biological chemistry - 15 Aug 2003

Volynski Kirill E, Capogna Marco, Ashton Anthony C, Thomson Derek, Orlova Elena V, Manser Catherine F, Ribchester Richard R, Ushkaryov Yuri A

Abstract excerpt

Alpha-latrotoxin (LTX) causes massive release of neurotransmitters via a complex mechanism involving (i) activation of receptor(s) and (ii) toxin insertion into the plasma membrane with (iii) subsequent pore formation. Using cryo-electron microscopy, electrophysiological and biochemical methods, we demonstrate here that the recently described toxin mutant (LTXN4C) is unable to insert into membranes and form pores...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acetylcholine
Share to Carbon Radioisotopes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Catecholamines

Share to Chromaffin Cells

Share to Exocytosis

Share to Neuromuscular Junction

Share to Protein Structure, Quaternary

Share to Synaptosomes

Source

Identifiers

PMID: 12782639
DOI: 10.1074/jbc.M210395200

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mutant alpha-latrotoxin (LTXN4C) does not form pores and causes secretion by receptor stimulation: this action does not require neurexins.PMID 12782639Read ↗

alpha-latrotoxin action probed with recombinant toxin: receptors recruit alpha-latrotoxin but do not transduce an exocytotic signal.Semantic proximity Read ↗

Latrophilin, neurexin, and their signaling-deficient mutants facilitate alpha -latrotoxin insertion into membranes but are not involved in pore formation.Semantic proximity Read ↗

alpha-Latrotoxin, acting via two Ca2+-dependent pathways, triggers exocytosis of two pools of synaptic vesicles.Semantic proximity Read ↗

Calcium-independent receptor for alpha-latrotoxin and neurexin 1alpha [corrected] facilitate toxin-induced channel formation: evidence that channel formation results from tethering of toxin to membrane.Semantic proximity Read ↗

Activation of alpha-latrotoxin receptors in neuromuscular synapses leads to a prolonged splash acetylcholine release.Semantic proximity Read ↗

Alpha-latrotoxin modulates the secretory machinery via receptor-mediated activation of protein kinase C.Semantic proximity Read ↗

Syntaxin requirement for Ca2+-triggered exocytosis in neurons and endocrine cells demonstrated with an engineered neurotoxin.Semantic proximity Read ↗

Transmembrane segments of syntaxin line the fusion pore of Ca2+-triggered exocytosis.Semantic proximity Read ↗

The transmembrane domain of syntaxin 1A negatively regulates voltage-sensitive Ca(2+) channels.Semantic proximity Read ↗

Isoflurane inhibits the neurotransmitter release machinery.Semantic proximity Read ↗

Signal transmission in ligand-gated receptors.Semantic proximity Read ↗

Irreversible block of cardiac mutant Na+ channels by batrachotoxin.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.