TY - JOUR
T1 - Herpes simplex virus type 2 US3 blocks apoptosis induced by sorbitol treatment
AU - Murata, Takayuki
AU - Goshima, Fumi
AU - Yamauchi, Yohei
AU - Koshizuka, Tetsuo
AU - Takakuwa, Hiroki
AU - Nishiyama, Yukihiro
N1 - Funding Information:
We would like to thank E. Iwata and T. Tsuruguchi for their technical support. This research was supported by a grant from the Japan Society for the Promotion of Science (JRPS-RFTF97L00703) and also by a Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Science and Culture of Japan.
PY - 2002
Y1 - 2002
N2 - Previously, we established HEp2 cell lines which express the US3 protein kinase of herpes simplex virus type 2 upon induction with IPTG. Using these cells, we examined whether expression of US3 is sufficient to protect cells from apoptotic cell death induced by sorbitol. Cells expressing US3 showed significantly reduced nuclear fragmentation in the degree that DNA fragmentation and caspase-3 activation were suppressed. It is known that stressors such as osmotic shock and UV irradiation induce the activation of the JNK (c-Jun N-terminal kinase), which can lead to apoptotic cell death. Expression of US3 resulted in the suppression of sorbitol-induced phosphorylation of JNK and MKK4/SEK1, suggesting that the suppression of apoptotic cell death was due to the attenuation of JNK activity.
AB - Previously, we established HEp2 cell lines which express the US3 protein kinase of herpes simplex virus type 2 upon induction with IPTG. Using these cells, we examined whether expression of US3 is sufficient to protect cells from apoptotic cell death induced by sorbitol. Cells expressing US3 showed significantly reduced nuclear fragmentation in the degree that DNA fragmentation and caspase-3 activation were suppressed. It is known that stressors such as osmotic shock and UV irradiation induce the activation of the JNK (c-Jun N-terminal kinase), which can lead to apoptotic cell death. Expression of US3 resulted in the suppression of sorbitol-induced phosphorylation of JNK and MKK4/SEK1, suggesting that the suppression of apoptotic cell death was due to the attenuation of JNK activity.
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U2 - 10.1016/S1286-4579(02)01590-3
DO - 10.1016/S1286-4579(02)01590-3
M3 - Article
C2 - 12067830
AN - SCOPUS:0036283307
SN - 1286-4579
VL - 4
SP - 707
EP - 712
JO - Microbes and Infection
JF - Microbes and Infection
IS - 7
ER -
