CLAC: a novel Alzheimer amyloid plaque component derived from a transmembrane precursor, CLAC-P/collagen type XXV

被引:168
作者
Hashimoto, T
Wakabayashi, T
Watanabe, A
Kowa, H
Hosoda, R
Nakamura, A
Kanazawa, I
Arai, T
Takio, K
Mann, DMA
Iwatsubo, T [1 ]
机构
[1] Univ Tokyo, Grad Sch Pharmaceut Sci, Dept Neuropathol & Neurosci, Tokyo 1130033, Japan
[2] RIKEN, Characterizat Ctr, Biomol Characterizat Div, Wako, Saitama 3510198, Japan
[3] Univ Tokyo, Grad Sch Med, Dept Neurol, Tokyo 1130033, Japan
[4] Sci Univ Tokyo, Fac Sci & Technol, Noda, Chiba 278, Japan
[5] Taisho Pharmaceut Co Ltd, Res Ctr, Omiya, Saitama 3308530, Japan
[6] Hope Hosp, Greater Manchester Neurosci Ctr, Salford M6 8HD, Lancs, England
关键词
Alzheimer's disease; amyloid; collagen;
D O I
10.1093/emboj/21.7.1524
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We raised monoclonal antibodies against senile plaque (SP) amyloid and obtained a clone 9D2, which labeled amyloid fibrils in SPs and reacted with similar to50/100 kDa polypeptides in Alzheimer's disease (AD) brains. We purified the 9D2 antigens and cloned a cDNA encoding its precursor, which was a novel type II transmembrane protein specifically expressed in neurons. This precursor harbored three collagen-like Gly-X-Y repeat motifs and was partially homologous to collagen type XIII. Thus, we named the 9D2 antigen as CLAC (collagen-like Alzheimer amyloid plaque component), and its precursor as CLAC-P/collagen type XXV. The extracellular domain of CLAC-P/collagen type XXV was secreted by furin convertase, and the N-terminus of CLAC deposited in AD brains was pyroglutamate modified. Both secreted and membrane-tethered forms of CLAC-P/collagen type XXV specifically bound to fibrillized Abeta, implicating these proteins in beta-amyloidogenesis and neuronal degeneration in AD.
引用
收藏
页码:1524 / 1534
页数:11
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