Requirement of myosin Vb.Rab11a.Rab11-FIP2 complex in cholesterol-regulated translocation of NPC1L1 to the cell surface.

作者: Bei-Bei Chu , Liang Ge , Chang Xie , Yang Zhao , Hong-Hua Miao

DOI: 10.1074/JBC.M109.034355

关键词:

摘要: Niemann-Pick C1-like 1 (NPC1L1) plays a critical role in the enterohepatic absorption of free cholesterol. Cellular cholesterol depletion induces transport NPC1L1 from endocytic recycling compartment to plasma membrane (PM), and replenishment causes internalization together with via clathrin-mediated endocytosis. Although has been characterized, other proteins involved are largely unknown. Most vesicular trafficking events dependent on cytoskeleton motor proteins. Here, we investigated roles microfilament microfilament-associated triple complex composed myosin Vb, Rab11a, Rab11-FIP2 PM. Interfering dynamics by pharmacological treatment delayed cell surface. Meanwhile, inactivation any component Vb·Rab11a·Rab11-FIP2 inhibited export NPC1L1. Expression dominant-negative mutants or decreased cellular uptake blocking These results suggest that efficient PM is complex.

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