Loss of Fas ligand-function improves survival in G93A-transgenic ALS mice

Journal of the Neurological Sciences

Volumn 251, Issue 1-2, 2006, Pages 44-49

  Petri, Susanne ^a,b   Kiaei, Mahmoud ^a   Wille, Elizabeth ^a   Calingasan, Noel Y ^a   Flint Beal, M ^a  

^a WEILL CORNELL MEDICAL COLLEGE   (United States)

^b HANNOVER MEDICAL SCHOOL   (Germany)

Author keywords

Amyotrophic lateral sclerosis; Apoptosis; Fas; Fas ligand; G93A transgenic mouse model; Motor neurons; Nitrotyrosine; nNOS

Indexed keywords

FAS LIGAND;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL DEATH; CONTROLLED STUDY; DEGENERATIVE DISEASE; FUNCTIONAL PROTEOMICS; MOTONEURON; MOUSE; NERVE CELL DEGENERATION; NEUROPATHOLOGY; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION; SIGNAL TRANSDUCTION; SURVIVAL RATE; TRANSGENIC MOUSE;

AGE FACTORS; AMYOTROPHIC LATERAL SCLEROSIS; ANIMALS; BEHAVIOR, ANIMAL; CELL COUNT; DISEASE MODELS, ANIMAL; FAS LIGAND PROTEIN; IMMUNOHISTOCHEMISTRY; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MOTOR ACTIVITY; MOTOR NEURONS; NITRIC OXIDE SYNTHASE TYPE I; PROBABILITY; SPINAL CORD; SUPEROXIDE DISMUTASE; SURVIVAL ANALYSIS; TYROSINE;

EID: 33751256823     PISSN: 0022510X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.jns.2006.08.013     Document Type: Article

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