ArticleInsect biochemistry and molecular biology2022
Characterization of two kdr mutations at predicted pyrethroid receptor site 2 in the sodium channels of Aedes aegypti and Nilaparvata lugens.
Article in Insect biochemistry and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Pyrethroid resistance in Aedes aegypti: genetic mechanisms worldwide, and recommendations for effective vector control.Parasites & vectors · 2025Review
- Plasticity in Gene Expression Patterns andInternational journal of molecular sciences · 2024Article
- A unique mechanism of transfluthrin action revealed by mapping its binding sites in the mosquito sodium channel.Insect biochemistry and molecular biology · 2024Article
- Toward Overcoming Pyrethroid Resistance in Mosquito Control: The Role of Sodium Channel Blocker Insecticides.International journal of molecular sciences · 2023Article
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- Insights into insecticide-resistance mechanisms in invasive species: Challenges and control strategies.Frontiers in physiology · 2022Review
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Authors and funding
6 authors at 5 institutions in 4 countries.
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Abstract
Pyrethroid insecticides prolong the opening of insect sodium channels by binding to two predicted pyrethroid receptor sites (PyR), PyR1 and PyR2. Many naturally-occurring sodium channel mutations that confer pyrethroid resistance (known as knockdown resistance, kdr) are located at PyR1. Recent studies identified two new mutations, V253F and T267A, at PyR2, which co-exist with two well-known mutations F1534C or M918T, at PyR1, in pyrethroid-resistant populations of Aedes aegypti and Nilaparvata lugens, respectively. However, the role of the V253F and T267A mutations in pyrethroid resistance has not been functionally examined. Here we report functional characterization of the V253F and T267A mutations in the Ae. aegypti sodium channel AaNa
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