Journal article
Presenilin-Mediated Modulation of Capacitative Calcium Entry
Neuron (Cambridge, Mass.), v 27(3), pp 561-572
01 Sep 2000
PMID: 11055438
Featured in Collection : UN Sustainable Development Goals @ Drexel
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.
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Details
- Title
- Presenilin-Mediated Modulation of Capacitative Calcium Entry
- Creators
- Andrew S Yoo - Massachusetts General HospitalIsaac Cheng - Harvard Medical SchoolSungkwon Chung - Sungkyunkwan UniversityTallessyn Z Grenfell - Massachusetts General HospitalHanmi Lee - Sungkyunkwan UniversityEunju Pack-Chung - Massachusetts General HospitalMelissa Handler - Brigham and Women's HospitalJie Shen - Brigham and Women's HospitalWeiming Xia - Brigham and Women's HospitalGiuseppina Tesco - Massachusetts General HospitalAleister J Saunders - Massachusetts General HospitalKai Ding - Brigham and Women's HospitalMatthew P Frosch - Brigham and Women's HospitalRudolph E Tanzi - Massachusetts General HospitalTae-Wan Kim - Massachusetts General Hospital
- Publication Details
- Neuron (Cambridge, Mass.), v 27(3), pp 561-572
- Publisher
- Elsevier
- Number of pages
- 12
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biology
- Web of Science ID
- WOS:000089601300019
- Scopus ID
- 2-s2.0-0033712477
- Other Identifier
- 991021448042004721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Neurosciences