Abstract：
: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 L1BR1 virus. A US3-rescued isolate of the L1B(-)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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Mori I,Goshima F,Koshizuka T,Koide N,Sugiyama T,Yoshida T,Yokochi T,Kimura Y,Nishiyama Ydoi
10.1016/j.neulet.2003.08.033keywords:
subject
Has Abstractpub_date
2003-11-20 00:00:00pages
201-5issue
3eissn
0304-3940issn
1872-7972pii
S0304394003009765journal_volume
351pub_type
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