Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice-Reference-Cited by-同舟云学术

Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice

Published:1997-01 Issue:1 Volume:3 Page:67-72
ISSN:1078-8956
Container-title:Nature Medicine
language:en
Short-container-title:Nat Med

Author:

Citron Martin,Westaway David,Xia Weiming,Carlson George,Diehl Thekla,Levesque Georges,Johnson-wood Kelly,Lee Michael,Seubert Peter,Davis Angela,Kholodenko Dora,Motter Ruth,Sherrington Robin,Perry Billie,Yao Hong,Strome Robert,Lieberburg Ivan,Rommens Johanna,Kim Soyeon,Schenk Dale,Fraser Paul,St George Hyslop Peter,Selkoe Dennis J.

Publisher

Springer Science and Business Media LLC

Subject

General Biochemistry, Genetics and Molecular Biology,General Medicine

Link

http://www.nature.com/articles/nm0197-67.pdf

Reference28 articles.

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2. Jarrett, J.T., Berger, E.P. & Lansbury, P.T., The carboxy terminus of the beta amyloid protein is critical for the seeding of amyloid formation: Implications for the pathogenesis of Alzheimer's disease. Biochemistry 32, 4693–4697 (1993).

3. Scheuner, D. et al. Secreted amyloid β-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease. Nature Med. 2, 864–870 (1996).

4. Yankner, B.A. New clues to Alzheimer's disease: Unraveling the roles of amyloid and tau. Nature Med. 2, 850–852 (1996).

5. Citron, M. et al. Inhibition of amyloid β-protein production in neural cells by the serine protease inhibitor AEBSF. Neuron 17, 171–179 (1996).

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