Abstract
Interferon (IFN) treatment of cells results in the induction of 2-5A-synthetases, double-stranded RNA-activated enzymes that produce unusual 5′-phosphorylated 2′,5′-linked oligoadenylates known as 2-5A. 2.5A activates a unique IFN-induced endoribonuclease, the 2-5A-dependent RNase (RNase L), that is capable of degrading both viral and cellular RNA. The expression cloning of 2-5A-dependent RNase is leading to meaningful analysis of the physiological functions of the 2-5A system. For example, expression in mouse cells of a dominant-negative mutant form of 2-5A-dependent RNase suppressed both the antiencephalomyocarditis virus and anticellular activities of IFN. Future investigations into this intriguing ribonuclease pathway promise to provide an intricate view into a molecular pathway of IFN action.
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