Activation of the IFN-inducible enzyme RNase L causes apoptosis of animal cells
Activation of the IFN-inducible enzyme RNase L causes apoptosis of animal cells
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DOI：
10.1006/viro.1997.8719
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发表时间：
1997-09-29
期刊：
影响因子：
3.7
通讯作者：
Esteban, M
中科院分区：
文献类型：
--
作者：
DiazGuerra, M;Rivas, C;Esteban, M
The interferon (IFN)-induced enzyme RNase L produced by a recombinant vaccinia virus (VV) causes death of mammalian cells with morphological and biochemical characteristics of apoptosis. Coexpression of 2-5A-synthetase enhances apoptosis induced by RNase L. Activation of endogenous RNase L by infection with a VV ts mutant (ts22) or with wild-type virus in the presence of the antipoxvirus drug isatin-beta-thiosemicarbezonel a treatment known to significantly increase the amount of double-stranded RNA late during infection, also causes pronounced apoptosis of infected cells. The effects observed with recombinant virus-derived RNase L or with the endogenous enzyme are specific, since apoptosis also occurs in cells derived from mice lacking the IFN-induced protein kinase (PKR). The apoptosis antagonist Bcl-2 prevents induction of cell death by RNase L activation. Apoptosis of mammalian cells by RNase L activation could be a mechanism mediating anticellular actions of IFN. (C) 1997 Academic Press.
