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Titlebook: Biochemical Sites of Insecticide Action and Resistance; Isaac Ishaaya Book 2001 Springer-Verlag Berlin Heidelberg 2001 Antagonist.Glutamat

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期刊全称Biochemical Sites of Insecticide Action and Resistance
影响因子2023Isaac Ishaaya
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发行地址Overview on the research progress over the past years in insecticide biochemistry.Includes supplementary material:
图书封面Titlebook: Biochemical Sites of Insecticide Action and Resistance;  Isaac Ishaaya Book 2001 Springer-Verlag Berlin Heidelberg 2001 Antagonist.Glutamat
影响因子In recent years many of the conventional methods of insect control by broad­ spectrum synthetic chemicals have come under scrutiny because of their unde­ sirable effects on human health and the environment. In addition, some classes of pesticide chemistry, which generated resistance problems and severely affected the environment, are no longer used. It is against this background that the authors of this book present up-to-date findings-relating to biochemical sites that can serve as targets for developing insecticides with selective prop­ erties, and as the basis for the elucidation of resistance mechanisms and countermeasures. The book consists of eight chapters relating to biochemical targets for insec­ ticide action and seven chapters relating to biochemical modes of resistance and countermeasures. The authors of the chapters are world leaders in pesti­ cide chemistry, biochemical modes of action and mechanisms of resistance. Biochemical sites such as chitin formation, juvenile hormone and ecdysone receptors, acetylcholine and GABA receptors, ion channels, and neuropeptides are potential targets for insecticide action. The progress made in recent years in molecular biology (pres
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https://doi.org/10.1007/978-3-662-46384-0by the present authors) and in .mosquitoes, where a similar increase in esterase activity was associated with insecticide resistance (recently reviewed by Hemingway and Karunaratne 1998). The first molecular genetic evidence supporting the hypothesis was with mosquitoes, when a large increase (ca. 2
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Acetylcholine Receptors as Sites for Developing Neonicotinoid Insecticides,icides that acted on the nAChR were of minor economic importance (<2% of the total insecticide market until 1991), and registered compounds were cartap (1964), bensultap (1968) and thiocyclam (1977). These compounds were metabolised in the insect’s body to nereistoxin, a naturally occurring toxin de
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Evolution of Amplified Esterase Genes as a Mode of Insecticide Resistance in Aphids,by the present authors) and in .mosquitoes, where a similar increase in esterase activity was associated with insecticide resistance (recently reviewed by Hemingway and Karunaratne 1998). The first molecular genetic evidence supporting the hypothesis was with mosquitoes, when a large increase (ca. 2
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Book 2001es of action and mechanisms of resistance. Biochemical sites such as chitin formation, juvenile hormone and ecdysone receptors, acetylcholine and GABA receptors, ion channels, and neuropeptides are potential targets for insecticide action. The progress made in recent years in molecular biology (pres
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Biochemical Sites of Insecticide Action and Resistance
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Biochemical Sites of Insecticide Action and Resistance978-3-642-59549-3
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ms of resistance. Biochemical sites such as chitin formation, juvenile hormone and ecdysone receptors, acetylcholine and GABA receptors, ion channels, and neuropeptides are potential targets for insecticide action. The progress made in recent years in molecular biology (pres978-3-642-64022-3978-3-642-59549-3
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