peptide metabolism
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2017 ◽  
Vol 139 (9) ◽  
pp. 3465-3472 ◽  
Author(s):  
Jun Onagi ◽  
Toru Komatsu ◽  
Yuki Ichihashi ◽  
Yugo Kuriki ◽  
Mako Kamiya ◽  
...  

2011 ◽  
Vol 25 (3) ◽  
pp. n/a-n/a ◽  
Author(s):  
Mark Farrell ◽  
Paul W. Hill ◽  
Sudas D. Wanniarachchi ◽  
John Farrar ◽  
Richard D. Bardgett ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Mallory Gough ◽  
Catherine Parr-Sturgess ◽  
Edward Parkin

Alzheimer's disease is a neurodegenerative condition characterized by an accumulation of toxic amyloid beta- (A-)peptides in the brain causing progressive neuronal death. A-peptides are produced by aspartyl proteinase-mediated cleavage of the larger amyloid precursor protein (APP). In contrast to this detrimental “amyloidogenic” form of proteolysis, a range of zinc metalloproteinases can process APP via an alternative “nonamyloidogenic” pathway in which the protein is cleaved within its A region thereby precluding the formation of intact A-peptides. In addition, other members of the zinc metalloproteinase family can degrade preformed A-peptides. As such, the zinc metalloproteinases, collectively, are key to downregulating A generation and enhancing its degradation. It is the role of zinc metalloproteinases in this “positive side of proteolysis in Alzheimer's disease” that is discussed in the current paper.


2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
TanYa M. Gwathmey ◽  
Hossam A. Shaltout ◽  
Patricia A. Nixon ◽  
James C. Rose ◽  
Lisa K. Washburn ◽  
...  

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