Mitochondrial apoptosis and the peripheral benzodiazepine receptor: a novel target for viral and pharmacological manipulation.
Mitochondrial apoptosis and the peripheral benzodiazepine receptor: a novel target for viral and pharmacological manipulation.
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DOI：
10.1084/jem.20021758
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发表时间：
2002-11-04
期刊：
影响因子：
--
通讯作者：
Kroemer G
中科院分区：
文献类型：
--
作者：
Castedo M;Perfettini JL;Kroemer G
病毒无情地利用它们的宿主细胞来保证它们自己的增殖和繁殖。为了实现这一目标，许多病毒抑制凋亡程序，从而避免宿主细胞的过早死亡。事实上，受感染细胞的凋亡可以被认为是对感染性病原体的原始防御，正如一个简单的Gedanken实验所示：如果所有宿主细胞在感染后立即死亡，那么病毒就不能复制。只有在病毒生命周期的晚期，一些病毒才在其宿主细胞中或通过各种不同的策略在免疫相关细胞中主动诱导细胞凋亡，其具体目的是破坏宿主的先天或同源免疫应答。随着病毒与宿主共同进化以适应特定的生态位，它们已经“学会”瞄准宿主细胞生物学中的战略过程。一个有趣的例子是现在由痘病毒引起的粘液瘤病，一种致命的疾病，已经消灭了整个兔子种群。粘液瘤病毒编码一种名为M11L的蛋白质，如本期（1）所示，该蛋白质通过作用于外周型苯二氮卓受体（PBR）来抑制宿主细胞凋亡。
Viruses mercilessly exploit their host cells to guarantee their own proliferation and propagation. To achieve this goal, many viruses suppress the apoptotic program, thereby avoiding premature death of the host cell. Indeed, apoptosis of infected cells may be considered as a pristine defense against infectious pathogens, as illustrated by a simple Gedankenexperiment: if all host cells died immediately after infection, then the virus could not replicate. It is only at late stages of the viral life cycle that some viruses actively induce apoptosis, either in their host cells or, via a variety of different strategies, in immunologically relevant cells, with the specific aim to subvert the host’s innate or cognate immune response. As viruses have coevoluted with their host to adapt to particular ecological niches, they have “learned” to target strategic processes in their host cell’s biology. One fascinating example is now provided by the poxvirus that causes myxomatosis, a lethal disease which has been eradicating entire populations of rabbits. Myxoma virus codes for a protein designated M11L, which, as shown in this issue (1), inhibits host cell apoptosis by acting on the peripheral-type benzodiazepine receptor (PBR).
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DOI：
10.1093/jnci/90.18.1400
发表时间：
1998-09-16
期刊：
JOURNAL OF THE NATIONAL CANCER INSTITUTE
影响因子：
--
作者：
Miccoli, L;Poirson-Bichat, F;Oudard, S
通讯作者：
Oudard, S
影响因子：
5.7
作者：
Verma, A;Facchina, SL;Snyder, SH
通讯作者：
Snyder, SH
影响因子：
4.8
作者：
Clarke, SJ;McStay, GP;Halestrap, AP
通讯作者：
Halestrap, AP
影响因子：
3.9
作者：
Goldmacher, VS
通讯作者：
Goldmacher, VS
影响因子：
4.8
作者：
Chen, M;Won, DJ;Gottlieb, RA
通讯作者：
Gottlieb, RA