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Earlier studies on macrophage-cholesterol crystal interaction have suggested sequestration of cholesterol crystals in surface-connected compartments [38], as well as complete phagocytosis of the crystals [39].
We found that disruption of lipid raft microdomains by nystatin sequestration of cholesterol both reduced rPrP membrane binding and blocked internalization, suggesting that extracellular rPrP was also directed to lipid raft microdomains and that localization to rafts was required for uptake of extracellular rPrP (Figure 1C).
Thus, in NPC disease, the primary reason for neuron death is generally considered to be the sequestration of cholesterol in late endosomes and/or lysosomes.
The repression of Muc2 induced by rVvpE was highly susceptible to the knockdown of intelectin-1b (ITLN) and sequestration of cholesterol by methyl- β-cyclodextrin.
The apoptotic cell death induced by rVvhA is highly susceptible to the sequestration of cholesterol by methyl- β-cyclodextrin, whereas for necrotic cell death, this shows a marginal effect.
Finally, intracellular sequestration of cholesterol, a relevant risk factor in AD [ 13], can as well promote abnormal endosomal trafficking/activity of amyloidogenic proteins, thus enhancing Aβ production [ 81, 119, 167].
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The gene-mutations give characteristic abnormalities in the intracellular transport of endocytosed cholesterol with sequestration of unesterified cholesterol in lysosomes and late endosomes.
The sequestration of free cholesterol into PrPSc-containing lipid rafts may deplete free cholesterol from other cellular pools where it helps to stabilise the packing of sphingolipids, gangliosides and raft-associated proteins in the membrane.
In addition to the sequestration of unesterified cholesterol, glycosphingolipids also accumulate in late endosomes and/or lysosomes of NPC-deficient cells.
One unique feature of MPG-EGFP transduction is that the sequestration of plasma membrane cholesterol increased cytosolic labeling of this fusion protein.
Cortical neurons that did persist with cholesterol storage were found to always accumulate GM3 ganglioside, whereas those neurons without GM3 lacked evidence of cholesterol sequestration [12].
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