Annexin A6 modulates TBC1D15/Rab7/StARD3 axis to control endosomal cholesterol export in NPC1 cells.
作者： Elsa Meneses-Salas , Ana García-Melero , Kristiina Kanerva , Patricia Blanco-Muñoz , Frederic Morales-Paytuvi
DOI: 10.1007/S00018-019-03330-Y
关键词:
摘要: Cholesterol accumulation in late endosomes is a prevailing phenotype of Niemann-Pick type C1 (NPC1) mutant cells. Likewise, annexin A6 (AnxA6) overexpression induces reminiscent NPC1 Here, we demonstrate that this cellular cholesterol imbalance due to AnxA6 promoting Rab7 inactivation via TBC1D15, Rab7-GAP. In cells, depletion and eventual activation was associated with peripheral distribution increased mobility endosomes. This accompanied by an enhanced lipid droplets acyl-CoA:cholesterol acyltransferase (ACAT)-dependent manner. Moreover, AnxA6-deficient Rab7-mediated rescue endosome-cholesterol export required the StAR-related transfer domain-3 (StARD3) protein. Electron microscopy revealed significant increase membrane contact sites (MCS) between ER cells lacking AnxA6, suggesting StARD3-dependent MCS formation. study identifies as novel gatekeeper controls regulation Rab7-GAP
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