The endoplasmic reticulum is the main site for caspase-3 activation following aluminum-induced neurotoxicity in rabbit hippocampus

Neuroscience Letters

Volumn 324, Issue 3, 2002, Pages 217-221

  Ghribi, Othman ^a   Herman, Mary M ^b   Savory, John ^a,c  

^a UNIVERSITY OF VIRGINIA   (United States)

^b NATIONAL INSTITUTE OF MENTAL HEALTH   (United States)

^c UNIVERSITY OF VIRGINIA HEALTH SYSTEM   (United States)

Author keywords

Aluminum; Apoptosis; Calnexin; Caspase 3; Cytosol; Endoplasmic reticulum; Hippocampus

Indexed keywords

ALUMINUM MALTOL; CALNEXIN; CASPASE 3; MARKER; PROTEIN P17; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BRAIN LEVEL; BRAIN REGION; CELL DEATH; CELL ORGANELLE; CONTROLLED STUDY; CYTOPLASM; CYTOSOL; ENDOPLASMIC RETICULUM; ENZYME ACTIVATION; ENZYME ASSAY; ENZYME LOCALIZATION; FEMALE; HIPPOCAMPUS; IMMUNOHISTOCHEMISTRY; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; PROTEIN TRANSPORT; RABBIT;

ANIMALS; APOPTOSIS; CALCIUM-BINDING PROTEINS; CALNEXIN; CASPASE 3; CASPASES; DISEASE MODELS, ANIMAL; ENDOPLASMIC RETICULUM; FEMALE; HIPPOCAMPUS; IMMUNOHISTOCHEMISTRY; MICROSCOPY, ELECTRON; NEURODEGENERATIVE DISEASES; NEURONS; NEUROTOXINS; ORGANOMETALLIC COMPOUNDS; PYRONES; RABBITS;

EID: 0037166054     PISSN: 03043940     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0304-3940(02)00147-7     Document Type: Article

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