痘苗病毒SPI-2（B13R）基因产物对细胞凋亡的保护作用。
Protection against apoptosis by the vaccinia virus SPI-2 (B13R) gene product.
作者信息
Dobbelstein M, Shenk T
机构信息
Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, New Jersey 08544-1014, USA.
出版信息
J Virol. 1996 Sep;70(9):6479-85. doi: 10.1128/JVI.70.9.6479-6485.1996.
Abstract
Vaccinia virus contains a gene, termed SPI-2 or B13R, that is closely related in its sequence to a potent inhibitor of apoptosis from cowpox virus (crmA). Infection by vaccinia virus protects HeLa cells against apoptosis that is induced by an immunoglobulin M antibody against the fas receptor or by tumor necrosis factor alpha. This effect is profoundly reduced when the SPI-2 gene is deleted. The SPI-2 gene, when transiently expressed in these cells, can also protect against apoptosis mediated by these agents. Given the similarity to crmA, it seems likely that SPI-2 functions in an analogous fashion, inhibiting the activity of ICE protease family members and blocking the onset of apoptosis.
摘要
痘苗病毒含有一个名为SPI-2或B13R的基因，其序列与来自牛痘病毒的一种有效的凋亡抑制剂（crmA）密切相关。痘苗病毒感染可保护HeLa细胞免受由抗fas受体的免疫球蛋白M抗体或肿瘤坏死因子α诱导的凋亡。当SPI-2基因缺失时，这种效应会大大降低。SPI-2基因在这些细胞中瞬时表达时，也可保护细胞免受这些因子介导的凋亡。鉴于与crmA的相似性，SPI-2似乎以类似的方式发挥作用，抑制ICE蛋白酶家族成员的活性并阻断凋亡的发生。
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