Isomerization and/or racemization at Asp23 of Aβ42 do not increase its aggregative ability, neurotoxicity, and radical productivity in vitro

Biochemical and Biophysical Research Communications

Volumn 366, Issue 3, 2008, Pages 745-751

  Murakami, Kazuma ^a   Uno, Mayumi ^a   Masuda, Yuichi ^a   Shimizu, Takahiko ^b,c   Shirasawa, Takuji ^b,d   Irie, Kazuhiro ^a  

^a KYOTO UNIVERSITY   (Japan)

^b TOKYO METROPOLITAN INSTITUTE OF GERONTOLOGY   (Japan)

^c TOKYO UNIVERSITY OF AGRICULTURE AND TECHNOLOGY   (Japan)

^d JUNTENDO UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

Author keywords

Aggregation; Alzheimer's disease; Amyloid; ESR; Isomerization; MTT; Neurotoxicity; PC12; Racemization; Thioflavin T

Indexed keywords

AMYLOID BETA PROTEIN[1-42]; ASPARTIC ACID;

ANIMAL CELL; ARTICLE; CHEMICAL REACTION; CONTROLLED STUDY; IN VITRO STUDY; ISOMERIZATION; MUTANT; NEUROFILAMENT; NEUROTOXICITY; NONHUMAN; PATHOGENESIS; PATHOLOGY; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN MODIFICATION; RACEMIZATION; RAT; WILD TYPE;

AMYLOID BETA-PROTEIN; ANIMALS; BINDING SITES; CELL SURVIVAL; DIMERIZATION; ISOMERISM; NEUROTOXINS; PC12 CELLS; PEPTIDE FRAGMENTS; PROTEIN BINDING; RATS; STRUCTURE-ACTIVITY RELATIONSHIP;

EID: 37549010347     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2007.12.009     Document Type: Article

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