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In support of the latter hypothesis, we observed that the recruitment of host late endosomes (LEs) and lysosomes is reduced in uis4<jats:sup>\u2212<\/jats:sup>parasites, which lack a parasitophorous vacuole membrane protein and arrest during liver-stage development. Analysis of parasite development in host cells deficient for late endosomal or lysosomal proteins revealed that the Niemann\u2013Pick type C (NPC) proteins, which are involved in cholesterol export from LEs, and the lysosome-associated membrane proteins (LAMP) 1 and 2 are important for robust liver-stage P. berghei growth. Using the compound U18666A, which leads to cholesterol sequestration in LEs similar to that seen in NPC- and LAMP-deficient cells, we show that the restriction of parasite growth depends on cholesterol sequestration and that targeting this process can reduce parasite burden in vivo. Taken together, these data reveal that proper LE and lysosome function positively contributes to liver-stage Plasmodium development.<\/jats:p>","DOI":"10.1091\/mbc.e16-07-0531","type":"journal-article","created":{"date-parts":[[2017,1,26]],"date-time":"2017-01-26T02:35:25Z","timestamp":1485398125000},"page":"726-735","source":"Crossref","is-referenced-by-count":52,"title":["Sequestration of cholesterol within the host late endocytic pathway restricts liver-stage<i>Plasmodium<\/i>development"],"prefix":"10.1091","volume":"28","author":[{"given":"Wiebke","family":"Petersen","sequence":"first","affiliation":[{"name":"Molecular Parasitology, Humboldt University, 10115 Berlin, Germany"},{"name":"Max Planck Institute for Infection Biology, 10117 Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Werner","family":"Stenzel","sequence":"additional","affiliation":[{"name":"Institute for Neuropathology, Charit\u00e9-Universit\u00e4tsmedizin, 10117 Berlin, 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