A new drug design strategy: Killing drug resistant bacteria by deactivating their hypothetical genes

IF 1.2 4区 环境科学与生态学 Q4 ENVIRONMENTAL SCIENCES Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis Pub Date : 2016-10-01 DOI:10.1080/10590501.2016.1236605
T. Wong, Jimmy Kuo
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引用次数: 2

Abstract

ABSTRACT Despite that a bacterial genome is complicated by large numbers of horizontally transferred (HT) genes and function unknown hypothetical (FUN) genes, the Genic-Transcriptional-Stop-Signals-Ratio (TSSR) of a genome shows that HT and FUN genes are complementary to all other genes in the genome. When HT or certain FUN genes are omitted from the Escherichia coli K-12 genome, its Genomic-TSSR value becomes totally incomparable to other E. coli strains. The Genic-TSSR correlation tree of a pathogen shows that some FUN genes would form a unique cluster. Removing these genes by site-specific mutation or gene-knockout should lead to the demise of this pathogen.
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一种新的药物设计策略:通过使假定的基因失活来杀死耐药细菌
尽管细菌基因组由大量水平转移(HT)基因和功能未知的假设(FUN)基因组成,但基因组的基因-转录-停止信号比(TSSR)显示HT和FUN基因与基因组中所有其他基因是互补的。当从大肠杆菌K-12基因组中剔除HT或某些FUN基因时,其基因组- tssr值完全无法与其他大肠杆菌菌株相比。病原菌的遗传- tssr相关树显示,一些FUN基因会形成一个独特的簇。通过位点特异性突变或基因敲除去除这些基因应该会导致这种病原体的死亡。
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来源期刊
CiteScore
4.60
自引率
0.00%
发文量
10
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