Protection against apoptosis by the vaccinia virus SPI-2 (B13R) gene product
Protection against apoptosis by the vaccinia virus SPI-2 (B13R) gene product
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DOI：
10.1128/jvi.70.9.6479-6485.1996
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发表时间：
1996-09-01
影响因子：
5.4
通讯作者：
Shenk, T
中科院分区：
文献类型：
--
作者：
Dobbelstein, M;Shenk, T
痘苗病毒含有一个称为 SPI-2 或 B13R 的基因，该基因的序列与牛痘病毒 (crmA) 的有效细胞凋亡抑制剂密切相关。痘苗病毒感染可保护 HeLa 细胞免受针对 fas 受体的免疫球蛋白 M 抗体或肿瘤坏死因子 α 诱导的细胞凋亡。当 SPI-2 基因被删除时，这种效应会大大减弱。 SPI-2 基因在这些细胞中瞬时表达时，还可以防止这些药物介导的细胞凋亡。鉴于与 crmA 的相似性，SPI-2 似乎可能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止细胞凋亡的发生。
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.