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无需敲门——克氏锥虫的细胞入侵策略。

Don't bother to knock--the cell invasion strategy of Trypanosoma cruzi.

作者信息

Tan Henry, Andrews Norma W

机构信息

Section of Microbial Pathogenesis and Dept of Cell Biology, Boyer Center for Molecular Medicine, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.

出版信息

Trends Parasitol. 2002 Oct;18(10):427-8. doi: 10.1016/s1471-4922(02)02368-1.

Abstract

The protozoan parasite Trypanosoma cruzi is responsible for Chagas disease, a serious debilitating disease that affects millions of people in Latin America. Trypomastigotes, the infective forms, are capable of invading and replicating in different cell types. The invasion process involves a gradual recruitment and fusion of host cell lysosomes at the parasite entry site, and is regulated by intracellular free Ca2+ transients triggered by trypomastigotes in host cells. This unusual, Ca2+-dependent lysosome exocytosis pathway was recently shown to be involved in the mechanism by which mammalian cells repair lesions on their plasma membrane.

摘要

原生动物寄生虫克氏锥虫是恰加斯病的病原体,恰加斯病是一种严重的使人衰弱的疾病,影响着拉丁美洲数百万人口。感染性形态的锥鞭毛体能够侵入不同类型的细胞并在其中复制。入侵过程涉及宿主细胞溶酶体在寄生虫进入部位的逐步募集和融合,并受锥鞭毛体在宿主细胞中触发的细胞内游离钙离子瞬变调节。最近研究表明,这种不同寻常的、依赖钙离子的溶酶体胞吐途径参与了哺乳动物细胞修复其质膜损伤的机制。

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