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NTE: One target protein for different toxic syndromes with distinct mechanisms?
Author(s) -
Glynn Paul
Publication year - 2003
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.10322
Subject(s) - toxicity , organophosphate , mutation , axon , biology , mechanism (biology) , gain of function , loss function , microbiology and biotechnology , chemistry , neuroscience , medicine , biochemistry , phenotype , philosophy , epistemology , pesticide , gene , agronomy
Epidemics of organophosphate‐induced delayed neuropathy (OPIDN) have paralysed thousands of people. This syndrome of nerve axon degeneration is initiated by organophosphates which react with neuropathy target esterase (NTE). Dosing experiments with adult chickens raise the possibility that OPIDN is initiated by a gain‐of‐function mechanism. By contrast, loss of NTE function by mutation causes massive apoptosis in Drosophila brain. Now, Winrow et al. show that nte −/− mice die by mid‐gestation, but nte +/− mice appear hyperactive and are more sensitive than wild‐type mice to a fatal form of OP toxicity.1 Thus, different toxic syndromes may be initiated via a single target protein. BioEssays 25:742–745, 2003. © 2003 Wiley Periodicals, Inc.