β1 and β3 subunits amplify mechanosensitivity of the cardiac voltage-gated sodium channel Nav1.5.
Action Potentials
/ physiology
Arrhythmias, Cardiac
/ metabolism
Cell Line
HEK293 Cells
Humans
Ion Channel Gating
/ physiology
Membrane Potentials
/ physiology
Myocytes, Cardiac
/ metabolism
NAV1.5 Voltage-Gated Sodium Channel
/ metabolism
Neurons
/ metabolism
Protein Subunits
/ metabolism
Sodium
/ metabolism
Cardiac ion channel
Mechanosensitivity
Patch-clamp
Sodium channel
Journal
Pflugers Archiv : European journal of physiology
ISSN: 1432-2013
Titre abrégé: Pflugers Arch
Pays: Germany
ID NLM: 0154720
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
25
05
2019
accepted:
21
10
2019
revised:
25
09
2019
pubmed:
16
11
2019
medline:
15
5
2020
entrez:
16
11
2019
Statut:
ppublish
Résumé
In cardiomyocytes, electrical activity is coupled to cellular contraction, thus exposing all proteins expressed in the sarcolemma to mechanical stress. The voltage-gated sodium channel Nav1.5 is the main contributor to the rising phase of the action potential in the heart. There is growing evidence that gating and kinetics of Nav1.5 are modulated by mechanical forces and pathogenic variants that affect mechanosensitivity have been linked to arrhythmias. Recently, the sodium channel β1 subunit has been described to stabilise gating against mechanical stress of Nav1.7 expressed in neurons. Here, we tested the effect of β1 and β3 subunits on mechanosensitivity of the cardiac Nav1.5. β1 amplifies stress-induced shifts of V
Identifiants
pubmed: 31728700
doi: 10.1007/s00424-019-02324-w
pii: 10.1007/s00424-019-02324-w
doi:
Substances chimiques
NAV1.5 Voltage-Gated Sodium Channel
0
Protein Subunits
0
SCN5A protein, human
0
Sodium
9NEZ333N27
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1481-1492Commentaires et corrections
Type : CommentIn
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