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ID 8296
Eprint ID
8296
フルテキストURL
Thumnail K002866.pdf 146 KB
タイトル(別表記)
G93A変異型ヒトSOD1トランスジェニックマウス脊髄における一過性低酸素刺激後の生存因子p-Akt,p-ERKの持続的誘導
著者
フリステリナ ストイチェバ イリエバ 岡山大学
抄録
Expression of survival p-AKT and p-ERK signals was examined by immunohistochemistry and Western blotting in the lumbar spinal cord of 12-week-old presymptomatic mice with human mutant G93A SOD1 gene (transgenic, Tg) and their wild-type (Wt) littermates during normoxia, and 0 and 6 h after 2 h of 9% hypoxia. During normoxia, a stronger p-AKT signal was detected in the nucleus of the motor neurons of Tg animals. At 0 h of recovery from 2 h of hypoxia, both p-AKT and p-ERK signals were induced at a slightly lower level in Tg (1.1-1.2-fold) compared to those of Wt (1.2-1.5-fold) animals. At 6 h of recovery, both p-AKT and p-ERK signals were sustained in the lumbar spinal motor neurons of Tg animals, while those in Wt animals quickly returned to baseline level. As a control, at 6 h of recovery, the hippocampus of Tg animals showed significantly sustained p-AKT levels, but not p-ERK levels, compared to Wt. The current results suggest that the presence of mutant SOD1 alters survival p-AKT and p-ERK signals, possibly to compensate for the acquired gain-of-function of the mutant protein.
キーワード
Amyotrophic lateral sclerosis (ALS)
Hypoxia
Phosphorylated serine/threonine kinase AKT (p-AKT)
Phosphorylated extracellular signal-regulated kinase (p-ERK)
Superoxide dismutase 1 (SOD1)
備考
http://dx.doi.org/10.1016/S0022-510X(03)00186-2
発行日
2005-03-25
出版物タイトル
資料タイプ
学位論文
学位授与番号
甲第2866号
学位授与年月日
2005-03-25
学位・専攻分野
博士(医学)
授与大学
岡山大学
オフィシャル URL
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14568129&dopt=Abstract
言語
Japanese
OAI-PMH Set
岡山大学
論文のバージョン
none
査読
不明