| How do presynaptic PLA2 neurotoxins block nerve terminals? | |
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MedLine Citation:
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PMID: 10838563 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Snake presynaptic neurotoxins with phospholipase A2 activity block nerve terminals in an unknown way. Here, we propose that they enter the lumen of synaptic vesicles following endocytosis and hydrolyse phospholipids of the inner leaflet of the membrane. The transmembrane pH gradient drives the translocation of fatty acids to the cytosolic monolayer, leaving lysophospholipids on the lumenal layer. Such vesicles are highly fusogenic and release neurotransmitter upon fusion with the presynaptic membrane, but cannot be retrieved because of the high local concentration of fatty acids and lysophospholipids, which prevents vesicle neck closure. |
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Authors:
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C Montecucco; O Rossetto |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Trends in biochemical sciences Volume: 25 ISSN: 0968-0004 ISO Abbreviation: Trends Biochem. Sci. Publication Date: 2000 Jun |
Date Detail:
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Created Date: 2000-07-21 Completed Date: 2000-07-21 Revised Date: 2012-02-22 |
Medline Journal Info:
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Nlm Unique ID: 7610674 Medline TA: Trends Biochem Sci Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 266-70 Citation Subset: IM |
Affiliation:
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Centro CNR Biomembrane and Dipartimento di Scienze Biomediche, Università di Padova, Via G. Colombo 3, 35121 Padova, Italy. cesare@civ.bio.unipd.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Elapid Venoms
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toxicity Models, Biological Nerve Endings / drug effects Neurons / drug effects* Neurotoxins / toxicity* Neurotransmitter Agents / metabolism Phospholipases A / metabolism* Phospholipases A2 Snake Venoms / metabolism* Synapses / metabolism Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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1068//Telethon |
| Chemical | |
Reg. No./Substance:
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0/Elapid Venoms; 0/Neurotoxins; 0/Neurotransmitter Agents; 0/Snake Venoms; 52019-39-3/taipoxin; EC 3.1.1.-/Phospholipases A; EC 3.1.1.4/Phospholipases A2 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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