Yeagle P L
Department of Biochemistry, University at Buffalo (SUNY), School of Medicine 14214.
Biochimie. 1991 Oct;73(10):1303-10. doi: 10.1016/0300-9084(91)90093-g.
The molecular basis for the essential role of cholesterol in mammalian (and other cholesterol-requiring) cells has long been the object of intense interest. Cholesterol has been found to modulate the function of membrane proteins critical to cellular function. Current literature supports two mechanisms for this modulation. In one mechanism, the requirement of 'free volume' by integral membrane proteins for conformational changes as part of their functional cycle is antagonized by the presence of high levels of cholesterol in the membrane. In the other mechanism, the sterol modulates membrane protein function through direct sterol-protein interactions. This mechanism provides an explanation for the stimulation of the activity of important membrane proteins and for the essential requirement of a structurally-specific sterol for cell viability. In some cases, these latter membrane proteins exhibit little or no activity in the absence of the specific sterol required for growth of that cell type. The specific sterol required varies from one cell type to another and is unrelated to the ability of that sterol to affect the bulk properties of the membrane.
长期以来，胆固醇在哺乳动物（以及其他需要胆固醇的）细胞中发挥重要作用的分子基础一直是人们密切关注的对象。已发现胆固醇可调节对细胞功能至关重要的膜蛋白的功能。当前的文献支持两种调节机制。在一种机制中，膜内在蛋白在其功能循环中进行构象变化所需的“自由体积”，会因膜中高水平胆固醇的存在而受到抑制。在另一种机制中，固醇通过直接的固醇 - 蛋白质相互作用来调节膜蛋白功能。这种机制解释了重要膜蛋白活性的刺激以及细胞活力对结构特异性固醇的基本需求。在某些情况下，这些膜蛋白在缺乏该细胞类型生长所需的特定固醇时，几乎没有或完全没有活性。所需的特定固醇因细胞类型而异，并且与该固醇影响膜整体性质的能力无关。
