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生物物理补偿机制缓冲大肠杆菌蛋白质 - 核酸相互作用以应对不断变化的环境。

Biophysical compensation mechanisms buffering E. coli protein-nucleic acid interactions against changing environments.

作者信息

Record M T, Courtenay E S, Cayley S, Guttman H J

机构信息

University of Wisconsin-Madison 53706, USA.

出版信息

Trends Biochem Sci. 1998 May;23(5):190-4. doi: 10.1016/s0968-0004(98)01207-9.

Abstract

Escherichia coli adapts to changes in growth osmolarity of at least 100-fold by making large changes in the amounts of intracellular water and solutes, including cytoplasmic K+. A wide range of in vitro salt, solute and biopolymer concentrations should therefore be considered 'physiological'. Paradoxically, these large, osmotically induced changes in cytoplasmic K+ concentration do not greatly affect the equilibria and kinetics of cytoplasmic protein-nucleic acid interactions. Biophysical effects resulting from changes in the amount of cytoplasmic water (such as macromolecular crowding) and in the concentrations of other cytoplasmic solutes appear to compensate for the effects of changes in cytoplasmic K+ concentration and thereby maintain protein-nucleic acid equilibria and kinetics in the range required for in vivo function.

摘要

大肠杆菌通过使细胞内水和溶质(包括细胞质中的钾离子)的含量发生大幅变化,来适应至少100倍的生长渗透压变化。因此,广泛的体外盐、溶质和生物聚合物浓度范围都应被视为“生理的”。矛盾的是,这些由渗透压诱导的细胞质钾离子浓度的大幅变化,并不会对细胞质中蛋白质-核酸相互作用的平衡和动力学产生很大影响。细胞质水量变化(如大分子拥挤效应)以及其他细胞质溶质浓度变化所产生的生物物理效应,似乎可以补偿细胞质钾离子浓度变化的影响,从而在体内功能所需的范围内维持蛋白质-核酸的平衡和动力学。

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