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Cholesterol depletion was achieved by metabolic inhibition of cholesterol synthesis in the absence of supplemental sterol, using compactin [22].
MβCD: cellular cholesterol depletion.
These domains exhibit increasing sensitivity to cholesterol depletion by methyl-β-cyclodextrin.
We further show that cholesterol depletion and antagonist treatment result in a reduced population of higher-order oligomers.
Intriguingly, disruption of clathrin lattices affected PrPC internalization in a manner similar to cholesterol depletion.
As shown in Fig. 1A, cholesterol depletion was dose-dependent for Vero and BHK-21 cells.
While lipid rafts are disrupted following cholesterol depletion, TEMs are resistant.
Cholesterol depletion results in decreased association of raft proteins and ultimately their associated functions.
Fig. 1B shows that insect cells were more affected by cholesterol depletion than mammalian cells.
Overall, LcJ amastigotes or serum opsonized hamster-derived amastigotes were not adversely affected by cholesterol depletion.
However, at high doses the cholesterol depletion is limiting, overwhelming any pro-vascular repair mechanism.
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