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Home: Papers of the Week
Annotation


Jankowsky JL, Slunt HH, Gonzales V, Savonenko AV, Wen JC, Jenkins NA, Copeland NG, Younkin LH, Lester HA, Younkin SG, Borchelt DR. Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease. PLoS Med. 2005 Dec;2(12):e355. PubMed Abstract, View on AlzSWAN

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  Comment by:  Tommaso Russo, ARF Advisor
Submitted 15 November 2005  |  Permalink Posted 17 November 2005
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REAGENTS/MATERIAL:

Immuno-blotting used the following antibodies: mouse monoclonal 22C11 (kind gift of Konrad Beyreuther and Andreas Weidemann) diluted 1:1,000, mouse monoclonal 6E10 (Signet Laboratories, Dedham, Massachusetts) diluted 1:2,500, rabbit polyclonal anti-superoxide dismutase 1 (m/hSOD1) diluted 1:2,500 to 1:4,000, or rabbit polyclonal CT15 (kind gift of Ed Koo; diluted 1:1,000.

For immunohistochemistry staining the following antibodies were used: primary antibody rabbit anti-Ab peptide polyclonal antibody, Zymed Laboratories, South San Francisco, California; rabbit anti-ubiquitin and rabbit anti–glial fibrillary acidic protein (GFAP) polyclonal antibodies, Dako, Carpinteria, California diluted 1:500 in TBS with 2% normal goat serum.

ELISA assay for human Ab used BAN50 for capture (epitope Ab1–16) and BA27 and BC05 for detection (Ab40 and Ab42, respectively) (Takeda Chemical Industries, Osaka, Japan). Total Ab (mouse + human; 1- to 1.5-mo samples only) was measured in each fraction using BNT77 for capture (epitope Ab11–28) and BA27 and BC05 for detection.

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