Expression of FasL and its interaction with Fas are mediated by c-Jun N-terminal kinase (JNK) pathway in 6-OHDA-induced rat model of Parkinson disease

Neuroscience Letters

Volumn 428, Issue 2-3, 2007, Pages 82-87

  Pan, Jing ^a,b   Zhao, Yan xin ^a   Wang, Zhi Quan ^b   Jin, Lei ^b   Sun, Zhi Kun ^a,b   Chen, Sheng Di ^a,b  

^a SHANGHAI SECOND MEDICAL UNIVERSITY   (China)

^b Chinese Academy of Sciences   (China)

Author keywords

Fas; FasL; Neuronal death; Substantia nigra pars compacta

Indexed keywords

FAS ANTIGEN; FAS LIGAND; OXIDOPAMINE; STRESS ACTIVATED PROTEIN KINASE;

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN INJURY; FEMALE; IMMUNOREACTIVITY; NERVE DEGENERATION; NONHUMAN; PARKINSON DISEASE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PROTEIN INTERACTION; RAT; SIGNAL TRANSDUCTION; SUBSTANTIA NIGRA;

ANIMALS; ANTIGENS, CD95; APOPTOSIS; BRAIN; CORPUS STRIATUM; DISEASE MODELS, ANIMAL; DOPAMINE; FAS LIGAND PROTEIN; FEMALE; JNK MITOGEN-ACTIVATED PROTEIN KINASES; NEURAL PATHWAYS; NEUROTOXINS; OXIDOPAMINE; PARKINSONIAN DISORDERS; RATS; RATS, SPRAGUE-DAWLEY; SIGNAL TRANSDUCTION; SUBSTANTIA NIGRA; SYMPATHOLYTICS; UP-REGULATION;

EID: 35748946322     PISSN: 03043940     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neulet.2007.09.032     Document Type: Article

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