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Effects of different anti-tau antibodies on tau fibrillogenesis: RTA-1 and RTA-2 counteract tau aggregation
Authors:Taniguchi Taizo  Sumida Miho  Hiraoka Shuko  Tomoo Koji  Kakehi Tomoko  Minoura Katsuhiko  Sugiyama Shigeru  Inaka Koji  Ishida Toshimasa  Saito Naoaki  Tanaka Chikako
Affiliation:Biosignal Research Center, Kobe University, Kobe, Hyogo 657-8501, Japan. tanigu@kobe-u.ac.jp
Abstract:Tau is the major antigenic component of neurofibrillary pathology in tauopathy, including Alzheimer's disease. Although conversion of soluble tau to an insoluble polymerized fibrillar form is a key factor in the pathogenesis of tauopathy, the mechanism of the change is unclear and no inhibitors of fibril formation are available. Monoclonal antibodies against the 1st or 2nd repeat of the microtubule binding domain, but not the C-terminal 16 residues, completely inhibited tau aggregation into PHF. Furthermore, they did not inhibit tau-induced tubulin assembly. Thus, they are useful to investigate tau protein conversion and will be useful therapeutic lead materials.
Keywords:ThS, thioflavin S   AD, Alzheimer disease   NFT, neurofibrillary tangle   PHF, paired helical filament   FTDP-17, frontotemporal dementia and Parkinsonism linked to chromosome 17   MBD, microtubule-binding domain   KLH, keyhole limpet hemocyanin   ELISA, enzyme-linked immunosorbent assay   MAP, microtubule-associated protein
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