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一个Kelch13定义的内细胞路径介导着疟疾寄生虫的抗素

Jakob Birnbaum¹, Sarah Scharf¹, Sabine Schmidt¹

¹Bernhard Nocht Institute for Tropical Medicine, Bernhard Nocht Str. 74, 20359 Hamburg, Germany.

Science (New York, N.Y.)

|January 4, 2020

概括

疟疾寄生虫对素的抵抗与血红蛋白吸收受损有关. 包括Kelch13在内的关键蛋白质控制了这一过程,影响了药物的激活和寄生虫的存活.

科学领域:

疟疾学
寄生虫学
抗药性机制

背景情况:

素衍生物 (ART) 是重要的抗疟疾药物.
由Kelch13突变引起的新兴ART耐药性威胁着疟疾控制.
凯尔奇13的确切功能及其在抗逆转录病毒耐药性的作用尚不完全清楚.

研究的目的:

阐明Kelch13蛋白的功能并确定其相互作用伙伴.
了解ART抗性的分子途径.
调查Kelch13与血红蛋白内细胞化和ART激活之间的联系.

主要方法:

蛋白质组分析以确定Kelch13定义的区间中的蛋白质.
疟疾寄生虫中已识别的蛋白质的遗传失活.
功能测试以评估血红蛋白内细胞和寄生虫对ART的反应.

主要成果:

包括Kelch13在内的8种蛋白质被确定为ART耐药性的关键途径.
这些蛋白质的无活化会对ART产生抗药性.
这些蛋白质对于血红蛋白内细胞分解至关重要,而在基尔奇13突变或失活的寄生虫中,这种降低.
降低的血红蛋白内细胞分解会影响ART的激活,从而导致抗药性.

结论:

涉及Kelch13及其相互作用的新途径对ART敏感性至关重要.
这种途径调节血红蛋白内细胞,直接影响ART激活.
了解这种途径为抗逆转录病毒耐药性疟疾提供了新的目标.

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