Formation of advanced glycation end-product-modified superoxide dismutase-1 (SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutation

Neuropathology

Volumn 21, Issue 1, 2001, Pages 67-81

  Kato, Shinsuke ^a   Nakashima, Kenji ^a   Horiuchi, Seikoh ^b   Nagai, Ryoji ^b   Cleveland, Don W ^c   Liu, Jian ^c   Hirano, Asao ^d   Takikawa, Miki ^a   Kato, Masako ^e   Nakano, Imaharu ^f   Sakoda, Saburo ^g   Asayama, Kohtaro ^h   Ohama, Eisaku ^a  

^a TOTTORI UNIVERSITY   (Japan)

^b KUMAMOTO UNIVERSITY   (Japan)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d MONTEFIORE MEDICAL CENTER   (United States)

^e TOTTORI UNIVERSITY   (Japan)

^f JICHI MEDICAL UNIVERSITY   (Japan)

^g OSAKA UNIVERSITY   (Japan)

^h UNIVERSITY OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH   (Japan)

Author keywords

Advanced glycation endproducts (AGE); Astrocytic hyaline inclusions (Ast HI); Familial amyotrophic lateral sclerosis (FALS); Granule coated fibrils; Maillard reaction; Neuronal Lewy body like hyaline inclusions (LBHI); Superoxide dismutase 1 (SOD1)

Indexed keywords

HYALIN; LYSINE; PENTOSIDINE; SUPEROXIDE DISMUTASE; UBIQUITIN;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; CELL INCLUSION; CELL ULTRASTRUCTURE; FAMILIAL DISEASE; GENE EXPRESSION; GENE MUTATION; GLYCATION; HUMAN; HUMAN TISSUE; IMMUNOELECTRON MICROSCOPY; IMMUNOHISTOCHEMISTRY; LEWY BODY; LYSOSOME; MOUSE; NERVE FIBER; NONHUMAN; PRIORITY JOURNAL; PROTEIN AGGREGATION; TRANSGENIC MOUSE;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMALS; GLYCOSYLATION END PRODUCTS, ADVANCED; HUMANS; INCLUSION BODIES; MICE; MICE, TRANSGENIC; MUTATION; SUPEROXIDE DISMUTASE;

EID: 17744397288     PISSN: 09196544     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1440-1789.2001.00359.x     Document Type: Article

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