Inhibition of Histone Deacetylation Enhances the Neurotoxicity Induced by the C-Terminal Fragments of Amyloid Precursor Protein

Journal of Neuroscience Research

Volumn 75, Issue 1, 2004, Pages 117-124

  Kim, Hye Sun ^a   Kim, Eun Mee ^a   Kim, Na Jung ^a   Chang, Keun A ^a   Choi, Yoori ^a   Ahn, Kwang Woo ^a   Lee, Jun Ho ^a   Kim, Seonghan ^a   Park, Cheol Hyoung ^a   Suh, Yoo Hun ^a  

^a Seoul National University   (South Korea)

Author keywords

AICD; Alzheimer's disease; C terminal fragment of amyloid precursor protein; Histone acetylation; Sodium butyrate

Indexed keywords

AMYLOID PRECURSOR PROTEIN; BUTYRIC ACID; HISTONE DEACETYLASE; HISTONE H3; HISTONE H4; NERVE GROWTH FACTOR;

ACETYLATION; ANIMAL CELL; APOPTOSIS; ARTICLE; CARBOXY TERMINAL SEQUENCE; CELL VIABILITY; CONTROLLED STUDY; CYTOTOXICITY; DEACETYLATION; GENETIC TRANSFECTION; IMMUNOHISTOCHEMISTRY; NERVE CELL DIFFERENTIATION; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; RAT; TRANSCRIPTION REGULATION;

ACETYLATION; AMYLOID BETA-PROTEIN PRECURSOR; ANIMALS; APOPTOSIS; BLOTTING, WESTERN; BUTYRATES; CELL DIFFERENTIATION; CELL SURVIVAL; CELLS, CULTURED; CEREBRAL CORTEX; DRUG INTERACTIONS; EMBRYO; ENZYME INHIBITORS; HISTONES; IMMUNOHISTOCHEMISTRY; IN SITU NICK-END LABELING; INDOLES; L-LACTATE DEHYDROGENASE; MOLECULAR STRUCTURE; NERVE GROWTH FACTOR; PC12 CELLS; RATS; RATS, SPRAGUE-DAWLEY; TRANSFECTION;

EID: 9144234107     PISSN: 03604012     EISSN: None     Source Type: Journal    
DOI: 10.1002/jnr.10845     Document Type: Article

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