A model of ischemia and reperfusion increases JNK activity, inhibits the association of BAD and 14-3-3, and induces apoptosis of rabbit spinal neurocytes

Neuroscience Letters

Volumn 473, Issue 3, 2010, Pages 196-201

  Fan, Jin ^a   Xu, Guangxu ^a   Nagel, David J ^b   Hua, Zhengzhe ^a   Zhang, Ning ^a   Yin, Guoyong ^a  

^a THE FIRST AFFILIATED HOSPITAL OF NANJING MEDICAL UNIVERSITY   (China)

^b UNIVERSITY OF ROCHESTER SCHOOL OF MEDICINE AND DENTISTRY   (United States)

Author keywords

BAD; Cytochrome c; Ischemia; JNK; Reperfusion; Spinal cord

Indexed keywords

CYTOCHROME C; PROTEIN 14 3 3; PROTEIN BAD; PROTEIN BCL 2; PROTEIN BCL XL; REGULATOR PROTEIN; SERINE; STRESS ACTIVATED PROTEIN KINASE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; CYTOPLASM; ENZYME ACTIVITY; ENZYME PHOSPHORYLATION; ENZYME RELEASE; HISTOPATHOLOGY; NONHUMAN; PRIORITY JOURNAL; PROTEIN LOCALIZATION; PROTEIN PROTEIN INTERACTION; REPERFUSION INJURY; SPINAL CORD INJURY; SPINAL CORD ISCHEMIA; SPINAL CORD NERVE CELL;

14-3-3 PROTEINS; ANIMALS; APOPTOSIS; BCL-ASSOCIATED DEATH PROTEIN; ISCHEMIA; MAP KINASE KINASE 4; MITOCHONDRIA; NEURONS; RABBITS; RANDOM ALLOCATION; REPERFUSION INJURY; SIGNAL TRANSDUCTION; SPINAL CORD;

EID: 77950339995     PISSN: 03043940     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neulet.2010.02.045     Document Type: Article

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