从大肠杆菌k - 12葡糖激酶的分子特征。
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迈耶D, Schneider-Fresenius C, Horlacher R, Peist R,嘘声W
从大肠杆菌k - 12葡糖激酶的分子特征。
J Bacteriol。1997年2月,179 (4):1298 - 306。
- PubMed ID
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9023215 (在PubMed]
- 文摘
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glk,葡糖激酶的结构基因的大肠杆菌,克隆和测序。超表达glk导致合成的胞质蛋白分子量为35000。酶的纯化,其动力学参数测定。葡萄糖和ATP的Km值分别为0.78和3.76毫米,分别。它的Vmax 158 U /毫克的蛋白质。构建了染色体glk-lacZ融合,并用于监控glk表达式。在所有条件下测试,只有增长葡萄糖glk的表达减少了约50%。beplayappfruR突变略glk-lacZ的表达增加,而过度的plasmid-encoded fruR +弱表达下降。FruR共识绑定主题123个基点上游发现了潜在的转录开始glk。过度的glk干扰麦芽糖的表达系统。 Repression was strongest in strains that exhibited constitutive mal gene expression due to endogenous induction and, in the absence of a functional MalK protein, the ATP-hydrolyzing subunit of the maltose transport system. It was least effective in wild-type strains growing on maltose or in strains constitutive for the maltose system due to a mutation in malT rendering the mal gene expression independent of inducer. This demonstrates that free internal glucose plays an essential role in the formation of the endogenous inducer of the maltose system.