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鼠伤寒沙门氏菌肠毒素基因的定位及基因产物的特性分析。

Location of the enterotoxin gene from Salmonella typhimurium and characterization of the gene products.

作者信息

Chary P, Prasad R, Chopra A K, Peterson J W

机构信息

Department of Microbiology, University of Texas Medical Branch, Galveston 77555-1051.

出版信息

FEMS Microbiol Lett. 1993 Jul 15;111(1):87-92. doi: 10.1111/j.1574-6968.1993.tb06366.x.

Abstract

The enterotoxin gene (stn) in Salmonella typhimurium (Q1 strain) was confined to an 800 bp ClaI-EcoRI genomic DNA fragment (pCE3) that coded for two polypeptides (25 and 12 kDa) under the control of the T7 RNA polymerase/promoter system. The appearance of the 25 kDa protein corresponded to the enterotoxic activity, as determined by elongation of Chinese hamster ovary (CHO) cells, fluid accumulation in rabbit intestinal loops, and altered vascular permeability in rabbit skin. The stn gene products (STN) caused an elevation of intracellular cAMP in CHO cells. These values were at control levels in stn mutants devoid of enterotoxicity, and the 25-kDa protein concurrently disappeared. The biological activity of the heat-labile enterotoxin was blocked by GM1 ganglioside and neutralized by affinity-purified antibodies made against cholera toxin. The 12 kDa protein however was not correlated with an enterotoxic response.

摘要

鼠伤寒沙门氏菌(Q1菌株)中的肠毒素基因(stn)局限于一个800 bp的ClaI-EcoRI基因组DNA片段(pCE3),该片段在T7 RNA聚合酶/启动子系统的控制下编码两种多肽(25 kDa和12 kDa)。通过中国仓鼠卵巢(CHO)细胞的伸长、兔肠袢中的液体蓄积以及兔皮肤中血管通透性的改变确定,25 kDa蛋白的出现与肠毒素活性相对应。stn基因产物(STN)导致CHO细胞内cAMP升高。在无肠毒素活性的stn突变体中,这些值处于对照水平,同时25 kDa蛋白消失。热不稳定肠毒素的生物活性被GM1神经节苷脂阻断,并被针对霍乱毒素制备的亲和纯化抗体中和。然而,12 kDa蛋白与肠毒素反应无关。

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