尿素酶
周质间隙
尿素
幽门螺杆菌
细胞质
生物化学
跨膜蛋白
化学
分子生物学
生物
大肠杆菌
遗传学
受体
基因
作者
David L. Weeks,Sepehr Eskandari,David R. Scott,George Sachs
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2000-01-21
卷期号:287 (5452): 482-485
被引量:509
标识
DOI:10.1126/science.287.5452.482
摘要
Acidic media trigger cytoplasmic urease activity of the unique human gastric pathogen Helicobacter pylori. Deletion of ureI prevents this activation of cytoplasmic urease that is essential for bacterial acid resistance. UreI is an inner membrane protein with six transmembrane segments as shown by in vitro transcription/translation and membrane separation. Expression of UreI in Xenopus oocytes results in acid-stimulated urea uptake, with a pH profile similar to activation of cytoplasmic urease. Mutation of periplasmic histidine 123 abolishes stimulation. UreI-mediated transport is urea specific, passive, nonsaturable, nonelectrogenic, and temperature independent. UreI functions as a H + -gated urea channel regulating cytoplasmic urease that is essential for gastric survival and colonization.
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