延胡索酸盐水平升高破坏结核分枝杆菌的氧化还原控制和生存能力。
Elevation of Fumarate Levels Compromise Redox Control and Viability in Mycobacterium tuberculosis.
机构信息
Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
出版信息
Cell Chem Biol. 2017 Mar 16;24(3):243-245. doi: 10.1016/j.chembiol.2017.03.003.
In this issue of Cell Chemical Biology, Ruecker et al. (2017) show that fumarase depletion in Mycobacterium tuberculosis leads to fumarate, a TCA cycle intermediate, accumulation, causing succination of a range of thiol-containing metabolites and proteins. Fumarate is bactericidal to the pathogen, and its accumulation may enhance the bactericidal effector mechanisms of other TCA cycle intermediates that accumulate due to activation of infected macrophages.
在本期《细胞化学生物学》中，Ruecker 等人（2017）表明，结核分枝杆菌中延胡索酸酶的耗竭会导致三羧酸 (TCA) 循环中间产物富马酸的积累，从而导致一系列含巯基代谢物和蛋白质的琥珀酰化。富马酸对病原体具有杀菌作用，其积累可能会增强由于感染的巨噬细胞激活而积累的其他 TCA 循环中间产物的杀菌效应机制。
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