Abstract:
:Nicastrin is a recently discovered protein interacting with presenilins and the beta-amyloid precursor protein, the proteins playing key roles in Alzheimer's disease and which, when mutated, appear responsible for early-onset familial forms of Alzheimer's disease. Nicastrin was reported to modulate beta-amyloid production, a phenotype affected differently by missense mutations or deletions of a conserved hydrophilic domain. In addition to such a function, nicastrin was recently suggested to possess putative catalytic activity based on its sequence homology with enzymes of the aminopeptidase family. We set up stably transfected human HEK293 cells expressing either wild-type or mutated nicastrins and we show that these proteins do not exhibit aminopeptidase M- and B-like activities.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Fergani A,Yu G,St George-Hyslop P,Checler Fdoi
10.1006/bbrc.2001.6030subject
Has Abstractpub_date
2001-12-07 00:00:00pages
678-80issue
3eissn
0006-291Xissn
1090-2104pii
S0006291X01960309journal_volume
289pub_type
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