Peroxiredoxin systems in mycobacteria.
Peroxiredoxin systems in mycobacteria.
复制标题
分枝杆菌中的过氧化还原蛋白系统。
作者：
T. Jaeger
像其他放线菌一样，结核分枝杆菌缺乏谷胱甘肽，因此，谷胱甘肽过氧化物酶在其哺乳动物宿主的抗氧化防御中占主导地位。病原体的过氧化氢代谢长期以来被认为依赖于含血红素的过氧化氢酶/过氧化物酶。缺乏过氧化氢酶的临床分离株是有毒的，并被证明对一线结核抑制剂异烟肼具有耐药性，因为该酶显然是激活这种药物所必需的。这些菌株的存活和毒性归因于过氧化物氧还蛋白型过氧化物酶烷基氢过氧化物还原酶（AhpC）和硫氧还蛋白过氧化物酶（TPx）。细菌中最常见的AhpC还原剂二硫还原酶AhpF在M中缺失。结核相反，AhpC可以被AhpD（一种含有CXXC基序的蛋白质）或分枝杆菌硫氧还蛋白之一TrxC还原。TPx被硫氧还蛋白B和C还原。分枝杆菌含有三种以上的过氧化物酶，1-Cys-Prx AhpE，Bcp和BcpB，其功能和还原剂仍然未知。
Like other actinomycetes Mycobacterium tuberculosis lacks glutathione and, consequently, the glutathione peroxidases that dominate the antioxidant defence of its mammalian hosts. The hydrogen peroxide metabolism of the pathogen has for long been recognised to depend on a heme-containing catalase/peroxidase. Clinical isolates lacking the catalase were virulent and proved to be resistant to the first line tuberculostatic isoniazid, because the enzyme is evidently required to activate this drug. The survival and virulence of such strains are attributed to the peroxiredoxin-type peroxidases alkyl hydroperoxide reductase (AhpC) and thioredoxin peroxidase (TPx). The most common AhpC reductant in bacteria, the disulfide reductase AhpF, is deleted in M. tuberculosis. Instead, AhpC can be reduced by AhpD, a CXXC-motif-containing protein, or by one of the mycobacterial thioredoxins, TrxC. TPx is reduced by thioredoxins B and C. Mycobacteria contain three more peroxiredoxins, the 1-Cys-Prx AhpE, Bcp and BcpB, whose function and reductants are still unknown.
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影响因子：
2.9
作者：
Ellis, HR;Poole, LB
通讯作者：
Poole, LB
影响因子：
2.8
作者：
Master, SS;Springer, B;Timmins, GS
通讯作者：
Timmins, GS
影响因子：
16
作者：
Chen, L;Xie, QW;Nathan, C
通讯作者：
Nathan, C
DOI：
10.1046/j.1432-1327.2000.01702.x
发表时间：
2000-10
期刊：
European journal of biochemistry
影响因子：
--
作者：
C. Williams;L. Arscott;S. Müller;B. Lennon;M. Ludwig;Pan‐Fen Wang;D. M. Veine;K. Becker;R. Schirmer
通讯作者：
C. Williams;L. Arscott;S. Müller;B. Lennon;M. Ludwig;Pan‐Fen Wang;D. M. Veine;K. Becker;R. Schirmer
影响因子：
3.9
作者：
Koshkin, A;Knudsen, GM;de Montellano, PRO
通讯作者：
de Montellano, PRO