Journal
NEUROSCIENCE LETTERS
Volume 351, Issue 3, Pages 201-205Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2003.08.033
Keywords
herpes simplex virus; US3 protein kinase; c-Jun N-terminal protein kinase; p38 mitogen-activated protein kinase; oxidative stress; apoptosis; piriform cortex
Categories
Ask authors/readers for more resources
Stereotaxic microinjection of herpes simplex virus (HSV) into the mouse olfactory bulb resulted in infection of neurons of the piriform cortex. Neurons infected with the wildtype HSV showed no evident phosphorylation of c-Jun N-terminal protein kinase (JNK)/c-Jun. In contrast, neurons infected with a US3 gene-disrupted mutant of the L1BR1 virus displayed phosphorylated JNK/c-Jun in a nuclear staining fashion. Induction of neuronal apoptosis by the wildtype HSV was partially suppressed when compared with that of the L I BR I virus. A US3-rescued isolate of the LIB- 11 virus behaved as did the wildtype virus. Collectively, the US3 protein kinase of HSV plays a role in attenuating the virus-induced activation of the JNK signal transduction pathway in the central nervous system and may contribute, at least in part, to controlling neuronal apoptosis. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available