期刊
TRAFFIC
卷 4, 期 9, 页码 581-586出版社
BLACKWELL MUNKSGAARD
DOI: 10.1034/j.1600-0854.2003.00117.x
关键词
endocytic fusion; exocytosis; intracellular survival; invasion; lipid salvage
类别
资金
- NIAID NIH HHS [R01 AI034036] Funding Source: Medline
Toxoplasma gondii is a widespread protozoan parasite that infects all nucleated cell types of warm-blooded vertebrates. Parasite motility is regulated by polymerization of new actin filaments that provide a substrate for the small myosin TgMyoA. Interaction between the cytoplasmic tails of parasite adhesins and the actin-binding protein aldolase links these cell surface proteins with the cytoskeleton. Translocation of adhesins coupled to extracellular receptors allows the parasite to glide across the substrate. This conserved system is important for active penetration into host cells and tissue migration by T. gondii . Entry into the host cell is accompanied by dramatic remodeling of the intracellular vacuole that the parasite resides in. This compartment resists fusion with host cell endocytic organelles, yet recruits mitochondria and endoplasmic reticulum in order to gain access to host cell nutrients. The combined abilities to actively penetrate host cells and control the fate of the parasite-containing vacuole contributes to the remarkable success of T. gondii as an intracellular parasite.
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