Activation of the IFN-inducible enzyme RNase L causes apoptosis of animal cells - PubMed (original) (raw)
. 1997 Sep 29;236(2):354-63.
doi: 10.1006/viro.1997.8719.
Affiliations
- PMID: 9325243
- DOI: 10.1006/viro.1997.8719
Free article
Activation of the IFN-inducible enzyme RNase L causes apoptosis of animal cells
M Díaz-Guerra et al. Virology. 1997.
Free article
Abstract
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-thiosemicarbazone, 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.
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