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新型抗生素天蓝霉素B对细菌细胞壁肽聚糖合成的抑制位点。

The site of inhibition of bacterial cell wall peptidoglycan synthesis by azureomycin B, a new antibiotic.

作者信息

Spiri-Nakagawa P, Oiwa R, Tanaka Y, Tanaka H, Omura S

出版信息

J Biochem. 1980 Aug;88(2):565-70. doi: 10.1093/oxfordjournals.jbchem.a133004.

Abstract

Azureomycin B (10 micrograms/ml), a new antibiotic from Pseudonocardia azurea nov. sp., caused the accumulation of lipid intermediate and inhibition of peptidoglycan synthesis in an invitro system using a particulate fraction from Bacillus megaterium KM with UDP-MurNAc-[3H]pentapeptide and cold UDP-GlcNac or cold UDP-MurNAc-pentapeptide and UDP-[3H]GlcNAc as substrates. At higher concentrations of azureomycin B (over 100 microgram/ml), lipid intermediate accumulation was also inhibited. When particulate fraction from Escherichia coli Y-10 and UDP-[14C[GlcNAc and cold UDP-MurNAc-pentapeptide were used, accumulation of lipid intermediate and inhibition of peptidoglycan synthesis were also observed. These results indicate that the primary target of azureomycin B is the transfer of the disaccharide peptide unit (GlcNAc-MurNAc-pentapeptide) from lipid-bound precursor to acceptor.

摘要

天蓝霉素B(10微克/毫升)是来自天蓝假诺卡氏菌新种的一种新型抗生素,在以巨大芽孢杆菌KM的颗粒部分为材料,以UDP-胞壁酰-[3H]五肽和冷UDP-葡萄糖胺或冷UDP-胞壁酰-五肽和UDP-[3H]葡萄糖胺为底物的体外系统中,它会导致脂质中间体的积累并抑制肽聚糖的合成。在较高浓度的天蓝霉素B(超过100微克/毫升)下,脂质中间体的积累也会受到抑制。当使用大肠杆菌Y-10的颗粒部分以及UDP-[14C]葡萄糖胺和冷UDP-胞壁酰-五肽时,也观察到了脂质中间体的积累和肽聚糖合成的抑制。这些结果表明,天蓝霉素B的主要作用靶点是二糖肽单元(葡萄糖胺-胞壁酰-五肽)从脂质结合前体向受体的转移。

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