Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
15 10 2019
15 10 2019
Historique:
received:
07
02
2019
accepted:
21
08
2019
entrez:
17
10
2019
pubmed:
17
10
2019
medline:
15
1
2020
Statut:
epublish
Résumé
Human primary aldosteronism (PA) can be caused by mutations in several ion channel genes but mouse models replicating this condition are lacking. We now show that almost all known PA-associated CLCN2 mutations markedly increase ClC-2 chloride currents and generate knock-in mice expressing a constitutively open ClC-2 Cl
Identifiants
pubmed: 31615979
doi: 10.1038/s41467-019-12113-9
pii: 10.1038/s41467-019-12113-9
pmc: PMC6794291
doi:
Substances chimiques
CLC-2 Chloride Channels
0
Chloride Channels
0
Clcn2 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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