The immunoproteasome 尾5i subunit is a key contributor to ictogenesis in a rat model of chronic epilepsy
详细信息 查看全文
- 作者：Michele Mishtoa ; b ; michele.mishto@charite.de" class="auth_mail" title="E-mail the corresponding author ; Muhammad L. Razac ; Dario de Biased ; Teresa Ravizzae ; Francesco Vasurif ; Morena Martuccid ; Christin Kellera ; Elena Bellavistad ; Tonia J. Buchholzg ; Peter M. Kloetzela ; Annalisa Pessionh ; Annamaria Vezzanie ; 1 ; Uwe Heinemannc ; 1
- 关键词：4-AP ; 4-aminopyridine ; Ach ; acetylcholine ; ACSF ; artificial cerebrospinal fluid ; CNS ; central nervous system ; i-proteasome ; immunoproteasome ; HMGB1 ; High Mobility Group Box-1 ; LPS ; lipopolysaccharide ; MCA ; 7-amino-4-methylcoumarin ; s-proteasome ; standard proteasome ; SE ; status epilepticus ; SLE ; seizure-like event ; TLE ; temporal lobe epilepsy ; TLR ; Toll-like receptor ; UPS ; ubiquitin&ndash ; proteasome system
- 刊名：Brain, Behavior, and Immunity
- 出版年：2015
- 出版时间：October 2015
- 年：2015
- 卷：49
- 期：Complete
- 页码：188-196
- 全文大小：1120 K
文摘
- •
Immunoproteasome 尾5i subunit is specifically induced in chronic epileptogenic foci.
- •
HMGB1-TLR4 axis may contribute to 尾5i subunit induction.
- •
Selective inhibition of 尾5i subunit activity mediates anti-ictogenic effects.
- •
尾5i subunit is a potential therapeutic target for seizure inhibition.