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细胞器掠夺:布鲁氏菌与内质网的相互作用

Organelle robbery: Brucella interactions with the endoplasmic reticulum.

作者信息

Celli Jean, Gorvel Jean-Pierre

机构信息

Centre d'Immunologie INSERM-CNRS-Université de la Méditerranée de Marseille-Luminy, Parc scientifique et technologique de Luminy, case 906, 13288 Marseille cedex 09, France.

出版信息

Curr Opin Microbiol. 2004 Feb;7(1):93-7. doi: 10.1016/j.mib.2003.11.001.

Abstract

Brucella is an intracellular pathogen that survives and multiplies inside host macrophages to cause brucellosis. The underlying mechanisms of intracellular survival, including the bacterial and the host determinants remain relatively unknown. Recent advances have helped to decipher how Brucella controls the biogenesis of its intramacrophagic replicative organelle. Brucella initially avoids or escapes the endocytic pathway to ensure its intracellular survival, which is then further secured via the biogenesis of an endoplasmic reticulum-derived replicative organelle. A major virulence factor, the VirB type IV secretion system, is required for sustained interactions and fusion with the host endoplasmic reticulum.

摘要

布鲁氏菌是一种细胞内病原体,它在宿主巨噬细胞内生存并繁殖,从而引发布鲁氏菌病。其细胞内存活的潜在机制,包括细菌和宿主决定因素,仍然相对未知。最近的进展有助于解读布鲁氏菌如何控制其巨噬细胞内复制细胞器的生物发生。布鲁氏菌最初避免或逃离内吞途径以确保其细胞内存活,随后通过内质网衍生的复制细胞器的生物发生进一步得到保障。一种主要的毒力因子,即VirB IV型分泌系统,是与宿主内质网持续相互作用和融合所必需的。

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