TASK-1 and TASK-3 channels modulate pressure overload-induced cardiac remodeling and dysfunction.
Animals
Cardiomegaly
/ genetics
Cardiomyopathies
/ genetics
Humans
Mice
Mice, Knockout
Myocardium
/ metabolism
Myocytes, Cardiac
/ metabolism
Nerve Tissue Proteins
/ genetics
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
/ genetics
Phosphorylation
Potassium Channels
/ genetics
Potassium Channels, Tandem Pore Domain
/ genetics
Proto-Oncogene Proteins c-akt
/ metabolism
Ventricular Remodeling
/ physiology
TASK channels
cardiac aging
cardiac function
cardiac hypertrophy
knockout mouse model
Journal
American journal of physiology. Heart and circulatory physiology
ISSN: 1522-1539
Titre abrégé: Am J Physiol Heart Circ Physiol
Pays: United States
ID NLM: 100901228
Informations de publication
Date de publication:
01 03 2020
01 03 2020
Historique:
pubmed:
25
1
2020
medline:
19
5
2020
entrez:
25
1
2020
Statut:
ppublish
Résumé
Tandem pore domain acid-sensitive K
Identifiants
pubmed: 31977249
doi: 10.1152/ajpheart.00739.2018
pmc: PMC7099448
doi:
Substances chimiques
Nerve Tissue Proteins
0
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
0
Potassium Channels
0
Potassium Channels, Tandem Pore Domain
0
Ppargc1a protein, mouse
0
TASK3 protein, mouse
0
potassium channel subfamily K member 3
1HQ3YCN4GS
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
H566-H580Subventions
Organisme : NHLBI NIH HHS
ID : K08 HL125905
Pays : United States
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