Journal
NEUROBIOLOGY OF DISEASE
Volume 13, Issue 3, Pages 238-245Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0969-9961(03)00035-4
Keywords
presenilin; beta-site APP cleaving enzyme (BACE1); amyloid; gamma-secretase; Alzheimer's disease
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Funding
- Canadian Institutes of Health Research [64309] Funding Source: Medline
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A neuropathological hallmark of Alzheimer's disease is the presence of amyloid plaques. The major constituent of these plaques, occurring largely in brain areas important for memory and cognition, is the 40-42 amyloid residues (Abeta). Abeta is derived from the amyloid protein precursor after cleavage by the recently identified beta-secretase (BACE1) and the putative gamma-secretase complex containing presenilin 1 (PS1). In an attempt to develop a functional secretase enzymatic assay in yeast we demonstrate a direct binding between BACE1 and PS1. This interaction was confirmed in vivo using coimmunoprecipitation and colocalization studies in human cultured cells. Our results show that PS1 preferably binds immature BACE1, thus possibly acting as a functional regulator of BACE1 maturation and/or activity. (C) 2003 Elsevier Science (USA). All rights reserved.
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