NTE: one target protein for different toxic syndromes with distinct mechanisms
NTE: one target protein for different toxic syndromes with distinct mechanisms
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DOI：
10.1002/bies.10322
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发表时间：
2003-08-01
期刊：
影响因子：
4
通讯作者：
Glynn, P
中科院分区：
文献类型：
--
作者：
Glynn, P
有机磷引起的延迟性神经病变（OPIDN）的流行已经使成千上万的人瘫痪。这种神经轴突变性综合征是由与神经病变靶酯酶（NTE）反应的有机磷引起的。对成年鸡进行的给药实验提高了OPIDN由功能获得机制启动的可能性。相反，NTE功能的突变导致果蝇大脑大量凋亡。现在，Winrow等人表明，nte（-/-）小鼠在妊娠中期死亡，但nte（+/-）小鼠表现出过度活跃，并且比野生型小鼠对一种致命形式的OP毒性更敏感。因此，不同的毒性综合征可能通过单一靶蛋白启动。(C) 2003 Wiley期刊有限公司
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. (C) 2003 Wiley Periodicals, Inc.