Activation of c‐Jun N‐terminal kinase during ischemia and reperfusion in mouse liver

FEBS Letters

Yamamoto, Ken-ichi¹  Yoshioka, Katsuji¹  Tani, Takashi²  Onishi, Ichiro¹  Hashimoto, Tetsuo²  Yagi, Masao²  Shimizu, Kouichi² 

[1]Department of Molecular Pathology, Cancer Research Institute, Kanazawa University, 13-1 Takaramachi, Kanazawa 920, Japan

[2]Department of Surgery II, School of Medicine, Kanazawa University, 13-1 Takaramachi, Kanazawa 920, Japan

关键词: Ischemia;    Signal transduction;    Mitogen-activated protein kinase;    c-Jun N-terminal kinase;    Stress-activated protein kinase;    JNK;    c-Jun N-terminal kinase;    SAPK;    stress-activated protein kinase;    MAPK;    mitogen-activated protein kinase;    TUNEL;    terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling;    GST;    glutathione S-transferase;    MBP;    myelin basic protein;   

DOI  :  10.1016/S0014-5793(97)01517-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We have generated a mouse model for hepatic ischemia in which surgical subcutaneous transposition of the spleen allows hepatic ischemia to be applied without affecting other tissues. Using this mouse model we investigated the relationship between the length of ischemic periods in the liver and subsequent liver function; furthermore, we assayed the activation of c-Jun N-terminal kinase (JNK) during ischemia and reperfusion. Although prior to this study only the activated form of JNK was known to be translocated to the nucleus, we found that JNK translocates to the nucleus during ischemia without activation and is then activated during reperfusion. These results suggest a novel mechanism of JNK activation.

【 授权许可】

Unknown