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大肠杆菌surE基因的突变会增加缺乏pcm修复甲基转移酶的菌株中异天冬氨酸的积累,但会抑制应激存活表型。

Mutations in the Escherichia coli surE gene increase isoaspartyl accumulation in a strain lacking the pcm repair methyltransferase but suppress stress-survival phenotypes.

作者信息

Visick J E, Ichikawa J K, Clarke S

机构信息

Department of Chemistry and Biochemistry, University of California, Los Angeles 90095-1569, USA.

出版信息

FEMS Microbiol Lett. 1998 Oct 1;167(1):19-25. doi: 10.1111/j.1574-6968.1998.tb13202.x.

Abstract

The Escherichia coli surE gene is co-transcribed with pcm, encoding the L-isoaspartyl protein repair methyltransferase, and is highly conserved among both the Eubacteria and the Archaea; however, no biochemical function has yet been identified for this gene. Isoaspartyl accumulation during stationary phase was much higher in a pcm surE double mutant than in either single mutant, suggesting that the two genes may represent two parallel pathways by which E. coli can respond to protein damage. A null mutation in surE also suppressed stress-survival defects previously observed in a pcm mutant strain, providing further evidence for an interaction between the two gene products.

摘要

大肠杆菌surE基因与pcm共同转录,pcm编码L-异天冬氨酰蛋白修复甲基转移酶,并且在真细菌和古细菌中都高度保守;然而,该基因的生化功能尚未确定。在稳定期,pcm surE双突变体中异天冬氨酰的积累比任何一个单突变体都高得多,这表明这两个基因可能代表大肠杆菌应对蛋白质损伤的两条平行途径。surE基因的无效突变也抑制了先前在pcm突变菌株中观察到的应激存活缺陷,为这两种基因产物之间的相互作用提供了进一步的证据。

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