Presenilins as endoplasmic reticulum calcium leak channels and Alzheimer’s disease pathogenesis
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1869-1889
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
online resource.
- Erschienen in
-
Presenilins as endoplasmic reticulum calcium leak channels and Alzheimer’s disease pathogenesis ; volume:54 ; number:8 ; day:24 ; month:7 ; year:2011 ; pages:744-751 ; date:8.2011
Science China / Life sciences. Life sciences ; 54, Heft 8 (24.7.2011), 744-751, 8.2011
- Urheber
-
Supnet, Charlene
- Beteiligte Personen und Organisationen
-
Bezprozvanny, Ilya
SpringerLink (Online service)
- DOI
-
10.1007/s11427-011-4201-y
- URN
-
urn:nbn:de:1111-201605232345
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
14.08.2025, 10:48 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Supnet, Charlene
- Bezprozvanny, Ilya
- SpringerLink (Online service)
Ähnliche Objekte (12)
Possible involvement of endoplasmic reticulum stress in the pathogenesis of Alzheimer’s disease
Mitochondrion to endoplasmic reticulum apposition length in zebrafish models of Alzheimer´s disease
Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model
Pharmacological Modulation of Ca2+ Leak through Sec61 Complexes of the Endoplasmic Reticulum
Complement in the pathogenesis of Alzheimer’s disease
N, N-Dimethyltryptamine, a natural hallucinogen, ameliorates Alzheimer’s disease by restoring neuronal Sigma-1 receptor-mediated endoplasmic reticulum-mitochondria crosstalk
Innate immunity and inflammation in Alzheimer´s disease pathogenesis
The plant endoplasmic reticulum
Correction to: Complement in the pathogenesis of Alzheimer’s disease
Identification of potential biomarkers for pathogenesis of Alzheimer’s disease
Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: recent advances
GJA1 (connexin43) is a key regulator of Alzheimer’s disease pathogenesis
Possible involvement of endoplasmic reticulum stress in the pathogenesis of Alzheimer’s disease
Mitochondrion to endoplasmic reticulum apposition length in zebrafish models of Alzheimer´s disease
Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model
Pharmacological Modulation of Ca2+ Leak through Sec61 Complexes of the Endoplasmic Reticulum
Complement in the pathogenesis of Alzheimer’s disease
N, N-Dimethyltryptamine, a natural hallucinogen, ameliorates Alzheimer’s disease by restoring neuronal Sigma-1 receptor-mediated endoplasmic reticulum-mitochondria crosstalk
Innate immunity and inflammation in Alzheimer´s disease pathogenesis
The plant endoplasmic reticulum
Correction to: Complement in the pathogenesis of Alzheimer’s disease
Identification of potential biomarkers for pathogenesis of Alzheimer’s disease
Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: recent advances
GJA1 (connexin43) is a key regulator of Alzheimer’s disease pathogenesis
Possible involvement of endoplasmic reticulum stress in the pathogenesis of Alzheimer’s disease
Mitochondrion to endoplasmic reticulum apposition length in zebrafish models of Alzheimer´s disease
Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model
Pharmacological Modulation of Ca2+ Leak through Sec61 Complexes of the Endoplasmic Reticulum
Complement in the pathogenesis of Alzheimer’s disease
N, N-Dimethyltryptamine, a natural hallucinogen, ameliorates Alzheimer’s disease by restoring neuronal Sigma-1 receptor-mediated endoplasmic reticulum-mitochondria crosstalk
Innate immunity and inflammation in Alzheimer´s disease pathogenesis
The plant endoplasmic reticulum
Correction to: Complement in the pathogenesis of Alzheimer’s disease
Identification of potential biomarkers for pathogenesis of Alzheimer’s disease
Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: recent advances