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Home: Papers of the Week
Annotation


Vogelsberg-Ragaglia V, Bruce J, Richter-Landsberg C, Zhang B, Hong M, Trojanowski JQ, Lee VM. Distinct FTDP-17 missense mutations in tau produce tau aggregates and other pathological phenotypes in transfected CHO cells. Mol Biol Cell. 2000 Dec;11(12):4093-104. PubMed Abstract


Corresponding Author: Virginia M. Y. Lee
Comments on Paper and Primary News
  Comment by:  Benjamin Wolozin, ARF Advisor (Disclosure)
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  I recommend this paper

"Important model of aggregation."

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Comments on Related Papers
  Related Paper: Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17.

Comment by:  Nikolaos K. Robakis
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This is an interesting paper as it offers a mechanism by which tau mutations may cause neuronal dysfunction in FTDP-1.

View all comments by Nikolaos K. Robakis
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REAGENTS/MATERIAL:
Site-directed mutagenesis (Quikchange kit; Stratagene) was used to created N279K, delta280K, P301L, S305N, V337M, R406W and triple mutation, VPR containing P301L, V337M and R406W) in Tau40 isoform. pSG5 vector (Stratagene) and Pfu DNA polymerase were used Rabbit polyclonal anti-tau 17026 (Pharmacia Biotech) for immunoprecipitation, 1:500 dilution. Alpha-tubulin MAb (Blose et al) for Immunofluorescence Fluroescent-labeled donkey anti-rabbit and Texas Red-labeled donkey anti-mouse IgG (Jackson Laboratories)

FUTURE DIRECTION:
Whether reduced binding of tau to MTs is an initiating even that leads to the formation of abnormal tau filaments Further experiments using CHO cell mutant tau model system to study the mechanisms leading to the formation of tau pathology in AD.

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