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. 2020 May 26;61(7):972–982. doi: 10.1194/jlr.R120000851

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Copyright © 2020 Sturley et al.

Published under exclusive license by The American Society for Biochemistry and Molecular Biology, Inc.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Fig. 3. — Representative cationic amphiphile drugs inhibit intracellular transport of cholesterol and mimic NP-C disease. Healthy patient fibroblasts were treated overnight with either the NPC1 inhibitor U18666A (5 μM) or NP-C disease mimetics chloroquine (10 μM) or progesterone (10 μM) and stained with filipin to visualize unesterified cholesterol. Images were obtained using a laser scanning spectral confocal microscope (Leica TCS SP-2). In all cases, U18666A, chloroquine, and progesterone phenocopy the biochemical hallmark of lysosomal cholesterol accumulation in NP-C patient fibroblasts. Cholesterol accumulation impairs lysosomal function, which may mediate the antiviral activity of the interventions discussed in this review.