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Journal of Virology, December 2004, p. 13132-13138, Vol. 78, No. 23
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.23.13132-13138.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

JNK Regulates the Release of Proapoptotic Mitochondrial Factors in Reovirus-Infected Cells

Departments of Neurology,¹ Immunology,² Neuroscience,³ Medicine and Microbiology, University of Colorado Health Sciences Center,⁵ Denver Veteran's Affairs Medical Center, Denver, Colorado,⁶ Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina⁴

Received 25 March 2004/ Accepted 19 July 2004

Reovirus-induced apoptosis is associated with activation of the proapoptotic mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) and the JNK-associated transcription factor c-Jun. Here we show that reovirus-induced apoptosis and activation of caspase 3 are inhibited in cells deficient in MEK kinase 1, an upstream activator of JNK in reovirus-infected cells. Inhibition of JNK activity following reovirus infection delays the release of proapoptotic mitochondrial factors and the subsequent onset of apoptosis. In contrast, reovirus-induced apoptosis is not blocked by infection with adenovirus expressing dominant-negative c-Jun, and c-Jun activation does not correlate with apoptosis in reovirus-infected cells. This is the first report demonstrating that JNK is associated with regulation of mitochondrial pathways of apoptosis following viral infection.

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