Wild-type and mutated nicastrins do not display aminopeptidase M- and B-like activities.

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.

authors

Fergani A,Yu G,St George-Hyslop P,Checler F

doi

10.1006/bbrc.2001.6030

subject

Has Abstract

pub_date

2001-12-07 00:00:00

pages

678-80

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006291X01960309

journal_volume

289

pub_type

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