TY - JOUR
T1 - Dephosphorylation of eNOS on Thr495 after transient forebrain ischemia in gerbil hippocampus
AU - Hashiguchi, Akihito
AU - Yano, Shigetoshi
AU - Morioka, Motohiro
AU - Hamada, Junichiro
AU - Kochi, Masato
AU - Fukunaga, Kohji
N1 - Funding Information:
This study was supported in part by Grants-in Aid for Scientific Research from the ministry of Education, Science, Sports and Culture of Japan (S.Y., M.M., and K.F.).
PY - 2005/2/18
Y1 - 2005/2/18
N2 - We investigated phosphorylation of endothelial nitric oxide synthase (eNOS) at two major sites, Ser1177 and Thr495, which has a critical role to control its activity, in the gerbil hippocampal microvasculature after transient forebrain ischemia. Ser1177 phosphorylation was unchanged by 24 h after reperfusion, despite post-ischemic up-regulation of eNOS protein. However, Thr495 phosphorylation significantly and persistently decreased by 48 h. We here defined the changes in eNOS phosphorylation in vivo following brain ischemia/reperfusion. (ischemia).
AB - We investigated phosphorylation of endothelial nitric oxide synthase (eNOS) at two major sites, Ser1177 and Thr495, which has a critical role to control its activity, in the gerbil hippocampal microvasculature after transient forebrain ischemia. Ser1177 phosphorylation was unchanged by 24 h after reperfusion, despite post-ischemic up-regulation of eNOS protein. However, Thr495 phosphorylation significantly and persistently decreased by 48 h. We here defined the changes in eNOS phosphorylation in vivo following brain ischemia/reperfusion. (ischemia).
KW - Cerebral ischemia
KW - Nitric oxide
KW - Phosphorylation
KW - eNOS
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U2 - 10.1016/j.molbrainres.2004.10.042
DO - 10.1016/j.molbrainres.2004.10.042
M3 - Article
C2 - 15710249
AN - SCOPUS:13844294075
VL - 133
SP - 317
EP - 319
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 2
ER -