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脂质流动性与膜蛋白动力学

Lipid fluidity and membrane protein dynamics.

作者信息

Lenaz G

机构信息

Department of Biology, University of Bologna, Italy.

出版信息

Biosci Rep. 1987 Nov;7(11):823-37. doi: 10.1007/BF01119473.

Abstract

Membrane fluidity plays an important role in cellular functions. Membrane proteins are mobile in the lipid fluid environment; lateral diffusion of membrane proteins is slower than expected by theory, due to both the effect of protein crowding in the membrane and to constraints from the aqueous matrix. A major aspect of diffusion is in macromolecular associations: reduction of dimensionality for membrane diffusion facilitates collisional encounters, as those concerned with receptor-mediated signal transduction and with electron transfer chains. In mitochondrial electron transfer, diffusional control is prevented by the excess of collisional encounters between fast-diffusing ubiquinone and the respiratory complexes. Another aspect of dynamics of membrane proteins is their conformational flexibility. Lipids may induce the optimal conformation for catalytic activity. Breaks in Arrhenius plots of membrane-bound enzymes may be related to lipid fluidity: the break could occur when a limiting viscosity is reached for catalytic activity. Viscosity can affect protein conformational changes by inhibiting thermal fluctuations to the inner core of the protein molecule.

摘要

膜流动性在细胞功能中起着重要作用。膜蛋白在脂质流体环境中是可移动的;膜蛋白的侧向扩散比理论预期的要慢,这是由于膜中蛋白质拥挤效应以及来自水相基质的限制。扩散的一个主要方面在于大分子缔合:膜扩散维度的降低促进了碰撞相遇,如那些与受体介导的信号转导和电子传递链相关的碰撞。在线粒体电子传递中,快速扩散的泛醌与呼吸复合物之间过量的碰撞相遇阻止了扩散控制。膜蛋白动力学的另一个方面是其构象灵活性。脂质可能诱导出催化活性的最佳构象。膜结合酶的阿伦尼乌斯图中的断点可能与脂质流动性有关:当达到催化活性的极限粘度时可能会出现断点。粘度可通过抑制蛋白质分子内核的热波动来影响蛋白质构象变化。

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