NTE: One target protein for different toxic syndromes with distinct mechanisms?

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<jats:title>Abstract</jats:title><jats:p>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 <jats:italic>Drosophila</jats:italic> brain. Now, Winrow et al. show that <jats:italic>nte<jats:sup>−/−</jats:sup></jats:italic> mice die by mid‐gestation, but <jats:italic>nte<jats:sup>+/−</jats:sup></jats:italic> mice appear hyperactive and are more sensitive than wild‐type mice to a fatal form of OP toxicity.<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#bib1">1</jats:ext-link> Thus, different toxic syndromes may be initiated via a single target protein. BioEssays 25:742–745, 2003. © 2003 Wiley Periodicals, Inc.</jats:p>

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  • BioEssays

    BioEssays 25 (8), 742-745, 2003-07-18

    Wiley

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