Regulation of the alternative β-secretase meprin β by ADAM-mediated shedding.
ADAM10
APP
Alzheimer’s disease
Meprin β
β-secretase
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
Aug 2019
Aug 2019
Historique:
received:
23
05
2019
accepted:
29
05
2019
revised:
23
05
2019
pubmed:
16
6
2019
medline:
30
7
2019
entrez:
16
6
2019
Statut:
ppublish
Résumé
Alzheimer's Disease (AD) is the sixth-leading cause of death in industrialized countries. Neurotoxic amyloid-β (Aβ) plaques are one of the pathological hallmarks in AD patient brains. Aβ accumulates in the brain upon sequential, proteolytic processing of the amyloid precursor protein (APP) by β- and γ-secretases. However, so far disease-modifying drugs targeting β- and γ-secretase pathways seeking a decrease in the production of toxic Aβ peptides have failed in clinics. It has been demonstrated that the metalloproteinase meprin β acts as an alternative β-secretase, capable of generating truncated Aβ
Identifiants
pubmed: 31201463
doi: 10.1007/s00018-019-03179-1
pii: 10.1007/s00018-019-03179-1
doi:
Substances chimiques
Amyloid beta-Peptides
0
Membrane Proteins
0
Presenilin-1
0
Serine Endopeptidases
EC 3.4.21.-
matriptase 2
EC 3.4.21.-
Metalloendopeptidases
EC 3.4.24.-
meprin B
EC 3.4.24.63
ADAM10 Protein
EC 3.4.24.81
Types de publication
Journal Article
Review
Langues
eng
Pagination
3193-3206Subventions
Organisme : Alzheimer Forschung Initiative (DE)
ID : 18007
Organisme : Deutsche Forschungsgemeinschaft (DE)
ID : 125440785 A9
Organisme : Deutsche Forschungsgemeinschaft (DE)
ID : 125440785 A15
Organisme : Deutsche Forschungsgemeinschaft (DE)
ID : BE 4086/2-2
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