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The interferon-induced double-stranded RNA-activated protein kinase induces apoptosis



The interferon-induced double-stranded RNA-activated protein kinase induces apoptosis



Virology 199(2): 491-496



Interferons (IFNs) exert antitumor activities, but the molecular mechanism underlying these effects is poorly understood. IFN-induced, double-stranded (ds) RNA-activated protein kinase (p68 kinase) has long been implicated in mediating the antiproliferative effects of IFN. In addition, recent studies suggest that p68 kinase may function as a tumor suppressor gene. In this investigation we showed that expression of p68 kinase in HeLa cells resulted in a rapid cell death characteristic of apoptosis. Rapid cell death was not observed in cells which expressed a mutant form of p68 kinase (lys-296 fwdarw arg) indicating that cell death observed is the result of p68 kinase expression and activation. Moreover, infection of HeLa cells with the mutant vaccinia virus lacking E3L gene, which encodes a dsRNA binding protein that acts as an inhibitor of p68 kinase, also resulted in apoptosis. Thus, we propose that human p68 kinase functions as a tumor suppressor gene by actively participating in apoptosis.

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Accession: 009593307

Download citation: RISBibTeXText

PMID: 7510087

DOI: 10.1006/viro.1994.1151



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