ABCA1: An Exit Strategy for CholesterolExcess

机译：ABCA1：胆固醇的退出策略

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Loss of function mutations in ABCA1 cause Tangier disease and familial hypoalphalipoproteinemia (Figure 1). These disorders are associated with a decreased ability to stimulated cholesterol removal from cells that have been incubated with aoplipoprotein A-L It is unclear how ABCA1 actually mediates cholesterol efflux and my lab has been interested in understanding this process. We have focused on understanding the structure of ABCA1, particularly its membrane topology (Figure 2). The initial ABCA1 cloned in 1994 was missing its first 60 amino acids and it was not until 6 years later that the full length of the transporter was determined. The extra 60 amino acids were at the amino terminus of the protein and contained a putative signal sequence (Figure 3).

机译：ABCA1中功能突变的丧失导致痴呆疾病和家族性低辐血性血症（图1）。这些疾病与刺激与Aoplipoprotein A-L一起孵育的细胞的刺激胆固醇去除的能力有关，目不是ABCA1实际介导胆固醇的浓缩症和我的实验室对理解这一过程感兴趣。我们专注于理解ABCA1的结构，特别是其膜拓扑结构（图2）。 1994年克隆的初始ABCA1缺少其前60个氨基酸，并且直到6年后，确定转运蛋白的全长。额外的60个氨基酸位于蛋白质的氨基末端并含有推定的信号序列（图3）。

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《World Association for Laser Therapy》|2002年||共24页
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1. ABCA1 modulates the oligomerization and Golgi exit of caveolin-1 during HDL-mediated cholesterol efflux in aortic endothelial cells. [J] . Lin YC, Lin CH, Kuo CY Biochemical and Biophysical Research Communications . 2009,第1期

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ABCA1: An Exit Strategy for CholesterolExcess

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