Logo image
Presenilin-Mediated Modulation of Capacitative Calcium Entry
Journal article   Open access   Peer reviewed

Presenilin-Mediated Modulation of Capacitative Calcium Entry

Andrew S Yoo, Isaac Cheng, Sungkwon Chung, Tallessyn Z Grenfell, Hanmi Lee, Eunju Pack-Chung, Melissa Handler, Jie Shen, Weiming Xia, Giuseppina Tesco, …
Neuron (Cambridge, Mass.), v 27(3), pp 561-572
01 Sep 2000
PMID: 11055438
url
https://doi.org/10.1016/S0896-6273(00)00066-0View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

We studied a novel function of the presenilins (PS1 and PS2) in governing capacitative calcium entry (CCE), a refilling mechanism for depleted intracellular calcium stores. Abrogation of functional PS1, by either knocking out PS1 or expressing inactive PS1, markedly potentiated CCE, suggesting a role for PS1 in the modulation of CCE. In contrast, familial Alzheimer's disease (FAD)–linked mutant PS1 or PS2 significantly attenuated CCE and store depletion–activated currents. While inhibition of CCE selectively increased the amyloidogenic amyloid β peptide (Aβ42), increased accumulation of the peptide had no effect on CCE. Thus, reduced CCE is most likely an early cellular event leading to increased Aβ42 generation associated with FAD mutant presenilins. Our data indicate that the CCE pathway is a novel therapeutic target for Alzheimer's disease.

Metrics

13 Record Views
289 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Neurosciences
Logo image