Abstract

Despite a tight regulation of its intracellular content, cholesterol is found accumulated in pathological conditions such as sphingolipidosis as well as after cell treatment with drugs like hydrophobic amines. Furthermore, cellular cholesterol increases when cultured cells approach confluence. Under these conditions, the endocytic pathways of plasma membrane sphingolipids are differently affected. In this short review, we will summarize recent results from our laboratory as well as those of other groups, indicating that the intracellular accumulation of cholesterol inhibits the dissociation of rab GTPases from the target membranes, causing the alteration of rab-mediated membrane traffic.

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